Q4 2020 Eledon Pharmaceuticals Inc Earnings Call
Greetings and welcome to the <unk> Pharmaceuticals fourth quarter, and full year 2020, operating and 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.
Anyone should require operator assistance during the conference. Please press star zero on your telephone keypad. As a reminder, this conference is being recorded I would now like to turn the conference over to your host Mr. John Kuwahara SVP of Finance. Please go ahead Sir.
Good afternoon, and thank you all for joining <unk> pharmaceuticals fourth quarter and full year 2020 financial results Conference call.
Joining me today are three members of our leadership team, David Alexandra Guo Chief Executive Officer, Steve Perrin, President and Chief Scientific Officer, and Paul Little Chief Financial Officer.
Earlier today <unk> issued a press release announcing financial results for the quarter and full year ended December 31 2020.
You may access the release under the investors tab on our company website <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 such forward looking statements are intended to be subject to the safe Harbor protection provided by the Reform Act.
The outcomes and results could differ materially from these forecasts due to the impact of many factors beyond the control of Ela Dawn.
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.
It just depends are directed to the risk factors set forth in <unk> reports filed with securities.
The Securities and Exchange Commission.
I would also like to note that celadon uses its investor relations website to publish important information about the company, including information that may be deemed material to investors financial and other information about Ela Dawn is keenly posted and is accessible on the company's investor Relations website at <unk> Dot com. It is now.
My pleasure to pass the call to our CEO, Dr. David Alexander growth Yeah.
Thank you John and good afternoon, everyone.
2020 was a transformational year for all of the dawn punctuated by our recent name change in January.
Our new name reflects the company's overall evolution, including our evolution and therapeutic focus to transplantation immune related diseases, and a myotrophin collateral soros's or a L. S.
This shift came as a result of a diligence and careful exploration of strategic alternatives to maximize shareholder value, which we concluded with the acquisition of analytics as therapeutics in September of last year.
Through this acquisition I'll, let dawn gains a new lead asset eight T 15 O. One a next generation anti CD 40 ligand antibody.
Steve will review shortly a T 15 O. One has unique attributes that we believe make it a potential best in class molecule targeting a well validated pathway that has shown promise in multiple indications.
Concurrent with the analytics. This transaction, we raised over $108 million in financing we plan on using the proceeds from this offering to advance phase two clinical trials of a T 15 O. One in up to four indications renal transplantation islet cell transplantation for the treatment of <unk>.
One diabetes autoimmune nephritis and day L S.
During the fourth quarter, we achieved multiple important milestones, we successfully launched and commenced patient enrollment of <unk> 15 O. One into a phase two way clinical trial for the treatment of adults with a L. S.
We then received clearance from health, Canada to proceed with initiation of a phase two clinical trial of a T 15, no one in islet cell transplantation for the treatment of type one diabetes.
These are important trials for us as a company and for these respective patient communities in a L. S average survival remains only 36 months after diagnosis for.
For type one diabetes, a T 15 O. One has the potential to help unlock a functional cure starting with some of the most at risk patients those with a brittle phase of the disease.
Finally.
We expanded the talent on our team in December we appointed Dr. June Lee to our board of Directors, a few weeks ago, we announced that Paul Little had joined as our Chief Financial Officer, and that Doctor, Jeff Bornstein will be joining us in early April as our Chief Medical Officer.
We are thrilled to have the opportunity to work with June Paul and Jeff and we look forward to benefiting from their extensive expertise.
I will now turn over the call to Steve Perrin, our President and Chief Scientific officer to discuss our clinical programs in more detail.
Afterwards, Paul Little will provide a financial update.
Steve. Please go ahead.
Thank you D a.
For those of you that are new to our non story I'll start off by giving a brief overview of our lead asset <unk> and ITG, one anti CD 40, logjam antibody blocking FC effector function.
Logically the interaction of CD 40, ligand and CD 40 results from clonal expansion antibody production and secretion of pro inflammatory cytokines, but amplify an immune response.
CD 40, CD 40 ligand pathway has been an attractive drug development target for decades because of the engagement of these receptors plays a pivotal role in immune system activation by meat eating both antibody and so we aren't immune responses to the modulation of germinal sole function. The clonal expansion of B cell from piece.
<unk>.
Antibody production in class switching as well as the polarization of pro inflammatory lymphocytes.
The initiation of a robust immune responses mitigated by co stimulatory signaling when CD 40 ligand binds co stimulatory receptor such as CD 40 on antigen presenting cells as these antigen presenting cells or simultaneously presenting foreign peptides from their MHC receptors to the T cell receptor.
<unk> on lymphocytes.
We are focusing our efforts on the development of an antagonist antibody targeting the ligand Robert from the receptor since targeting the ligand has been shown to be more efficacious and preclinical models of auto immunity and as well as the prevention of acute and long term allograph transplant rejection.
There may be three biological mechanisms for the benefit in preclinical ethically showed by targeting anti CD 40 ligand over targeting the CD 40 receptor the.
The first is differences in sell your distributions since the ligand is more restricted and its expression present on platelets and offer you'll salsa and activated lymphocytes.
First the receptors present more broadly on all antigen presenting cells, including monocytes macrophages dendritic cells and specialized antigen presenting cells and tissues. A second is that targeting both the receptor and the ligand inhibits b cell activation in class switching as well as inhibiting the pro inflammatory polarization of <unk>.
C D. Four positive T cells, however, blocking city 40 Y Gen also inhibits other integrin receptors, including city 11 receptors on antigen presenting cells doesn't blocking the pro inflammatory polarization of CDA positive cytotoxic T cells as well.
And finally third blocking the ligand also pulverized the CD four positive lymphocytes to become Fox P. Three positive T regs, thus potentially creating a more tolerant of environments in the context of preventing hours raft transplant rejection as well as auto immunity.
We plan to advance <unk>, one an up to four phase two clinical trials for prevention of kidney allograft rejection the.
The prevention of islet cell allograft rejection, autoimmune nephritis and AOS.
We selected these indications based on preclinical data that was generated with either our molecule or historical anti CD 40 ligand antibodies.
Preclinical data in animal disease models suggest a blocking C. D 40 ligand is the most efficacious way to prevent acute and long term transplant rejection in renal cell transplant and in some cases can induce long term transplant tolerance.
Blocking CD 40 ligand has been shown to be more effective at preventing allograft transfer rejection competitor blocking C. D 40 receptor importantly, targeting CD 40 ligand is not associated with systemic lymphopenia.
The ability to prevent acute and current transplant rejection and the absence of Calcine earn inhibitors has the potential to transform the clinical management to preventing graft rejection, thus potentially mitigating the net for toxicity cardio toxicity induction of diabetes and increased opportunities infections associated with calcium from the hip.
<unk> or C&I.
Chronic exposure to C&I is in organ transplantation is associated with an increase in type one diabetes. This is due to the toxicity of C&I is on insulin producing beta cells from the pancreas.
Similarly seen ours are toxic to transplants islet cells.
I Wouldnt cell transplantation up to 50 per cent of the transplanted islet cells may die within days after transplant transplantation in part due to C&I toxicity, thus exposing subjects to risk of transplant rejection and requiring multiple islet cell transplants in order to obtain a sufficient sell mass to eliminate the requirement for exogenous insulin.
Adoption of violence, all transplant as a treatment option.
And potential functional cure for brittle diabetes has therefore been hampered in part by the toxicity associated with the C&I as that are required to prevent I went so rejection net result in acute I'll, let so lawson dysfunction.
We believe that as a result, replacing C&I is with $80. If you know one may improve islet cell survival and clinical outcomes of surgeries associated with islet cell transplant, thus potentially allowing for islet cell transplants would become a viable treatment option and even a potential functional cure for persons who are living with type one diabetes.
And autoimmunity, we're focused on autoimmune and <unk>, which are autoimmune diseases of the kidney.
There was a long history of preclinical and clinical data demonstrating the blocking C. D 40, widening signaling ameliorates disease progression modifies biomarkers of disease, and improves renal function and diseases, such as focal segmental glomerular sclerosis or F. S. T S lupus nephritis and Iga Nephropathy for example.
Moreover, soluble CD 40 ligand, often correlates with disease flares in autoimmune diseases such as these.
Two clinical development program and they also was based on positive preclinical data in a rodent model of AOS conducted at the Aol's therapy Development Institute, our Atlas T G I.
<unk> has screened approximately 500 compounds in rodent models of ALS and according to a O S. T D. I blocking C. D 40 ligand function as one of only a handful of drugs that slows down disease progression improved survival and improved muscle function.
Similarly, how see similarly, how soluble CD 40 ligand can correlate with flares in autoimmune diseases soluble CD 40 ligand can also correlate with disease progression in a loss.
Shifting to our clinical trials.
Non initiated a phase two study of <unk> 51, and people living with a loss in October of 2020. The trial is a 12 week open label dose escalating safety and biomarker marker study with four doses of 850 no one.
This is the first multiple ascending dose study of <unk> 51 in humans. Thus the primary endpoint of this study is safety and Tolerability. We will also assess multiple exploratory biomarker endpoints, including target engagement pro inflammatory signaling in search of circulation such as TNF Alpha IL, six and euro filament light chain levels.
As a surrogate marker of neuro in health and disease progression.
Finally, we've been looking at some exploratory efficacy endpoints related to disease progression interest as changes in ALS functional rating scale or a lessor for us as well as for sportswear function. Although these are not expected to significantly change and a 12 week clinical study.
Despite the recent peaks in COVID-19 enrollment in this trial continues to be on track and we anticipate reporting on top line data from this trial in the first half of 2021.
In November of last year, we received clearance from health, Canada to proceed with the initiation of a phase II clinical trial of <unk> hundred one I would cell transplantation for type one diabetes.
This is a single arm open label study with primary endpoints assessing safety and Tolerability.
Glucose control and insulin independence reduction in HBA, one see in graft survival and people with type one diabetes.
We'll also be assessing hypoglycemic awareness events as well as renal function.
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 re initiating and performing these transplants in February of 2021.
Despite this COVID-19 related delay, we now expect our first patient to enroll in the second quarter of 2021, and we still anticipate that we'll be able to generate interim data and what cell transplant as planned in the first half of 2022.
In terms of renal transplantation pending regulatory clearance, including from the FDA, we target to initiate the phase II clinical trial clinical trial at the end of the second quarter 2021.
And finally, we'll discuss our specific fourth indication after we initiated the renal transplantation study.
With regards to releasing data, we looked forward to having presentations and posters at the American transplant conference in June.
We plan to present data from the phase one clinical study of <unk> as well as preclinical data, including characterization of <unk> 15, and wanted to in vitro assays and non human Primate studies of <unk> 51 in the prevention of islet cell transplant rejection.
Let me now turn the call over to our Chief Financial Officer, 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-K, which we'll file later today the.
The company reported a net loss of $5 9 million or $2 13 per share for the three months ended December 31, 2020, compared to a net loss of $4 1 million or $5 75 per share for the same period in 2019.
Research and development expenses were $3 million for the three months ended December 31, 2020, compared to $1 3 million for the comparable period in 2019.
General and administrative expenses were $3 3 million for the three months ended December 31, 2020, compared to $1 million for the comparable period in 2019.
Turning to a few key financial metrics for the full year.
We reported a net loss of $22 8 million or $15 72 per share for the year ended December 31, 2020, compared to a net loss of $16 million or $24 42 per share for the year ended December 31, 2019, R&D expenses were $6 1 million for the year ended December.
31, 2020 compared to $8 1 million for the year ended December 31 2019.
G&A expenses were $10 1 million for the year ended December 31, 2020, compared to $6 1 million for the year ended December 31 2019.
The company had approximately $114 2 million in cash and cash equivalents as of December 31, 2020, compared to $8 8 million in cash and cash equivalents as of December 31 2019.
Concurrent with our predecessor companies acquisition and Alexis Therapeutics in September 2020, we raised gross proceeds of $108 million through a private placement of share as to several highly regarded institutional investors.
Based on our current clinical and operating plan, we believe our current cash resources will fund operations well into 2023.
As is common for biotechs of our size and with our current <unk> expiring in the coming months, we are filing a new S. Three and establishing an at the market equity equity facility or ATM.
As <unk> indicated earlier, we're well financed to advance up to four clinical trials of <unk> hundred one and fund our operations as currently planned well into 2023.
However, we believe this ATM as prudent financial housekeeping and gives us the flexibility to raise additional capital should circumstances arise that would allow us to do so on terms favorable to the company.
<unk> has no obligation to sell shares under the ATM and we currently have no plans to utilize either the shelf or the ATM.
With that financial update let me turn the call back over to day.
Thank you Paul.
We are excited to close out a transformational year in 2028.
A year, where we acquired <unk> therapeutics completed a private placement financing.
With a blue chip group of investors advanced <unk> 15 O one into our first phase III trial in adults with a L. S and received clearance from health, Canada to proceed with initiation of our phase II clinical trial of 815 O. One in islet cell transplantation for type one diabetes.
Now with a L. S enrollment continuing multiple phase II trials planned to start this year pending clearances from regulatory agencies and are planning to present data on our work to date, starting without the American transplant Congress in June we believe we have set the stage for news.
Potentially value creating catalysts.
This year and next.
With that I will now ask the operator to begin our Q&A session.
Operator.
Thank you at this time, we'll be conducting a question and answer session. If you'd like to ask a question. Please press star one on your telephone keypad.
Non formation tone will indicate your line is in the question 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.
Your first question comes from the line of Alithia Young with Cantor. Please proceed with your question.
Hey, guys. Thanks for taking my questions and congrats on a good amount of progress that you've made over 'twenty 'twenty a couple of things from me just one.
For good channel once you can talk a little bit about what indications you might prefer.
You know as lip is kind of the lead one or they can the others just thinking about where kind of you know they're now from Lukas Johnson the market. The second question is.
Have there been have you provided any kind of evidence around target engagement.
Hum either like the sad study or anything and then the last question is just can you just talk a little bit about kind of the dynamics, which have been underpinning transplant trials during COVID-19. Thank you.
And we did day, thank you very much for the questions.
So maybe I'll start with the first one and then I'll turn it over to Steve to talk about.
Target engagement as well as ongoing dynamics.
In terms of the autoimmune indications.
We are looking at.
And indications in autoimmune nephritis, so as we mentioned autoimmune disease of the kidney there are three primary types of autoimmune.
Brightest that we're considering lupus nephritis, which you mentioned.
As well as <unk> and Iga nephropathy.
There's a good amount of.
Oracle preclinical data in the space of using anti CD 40.
Two.
To tackle these these indications and at this stage.
During that this would be our potential fourth.
Trial that we'd be starting we haven't finalized which specific indication we'd be going after.
In part because as you mentioned this is a rapidly evolving field.
So with that let me turn it over to Steve to talk about target engagement as well as.
What we're seeing.
With COVID-19 impact.
Sure. Thanks, Sean.
So on target engagement than we did in our phase one study for <unk>.
Highest dose just one of the doses eight Meg per kg.
Doing immune challenge with KLA, each and we showed that we can attenuate and immune response with the Calix challenge, we completely attenuated in two or three people.
So that was a very good demonstration to us that we had target engagement, because we completely blocked and antibody response to a foreign antigen.
On the third question as far as COVID-19 impacting transplant studies.
I guess, there's a couple of pieces of data there so although the site in Canada, and Alberta did shut down temporarily for islet cell during the peak of what we consider the Covid spike.
Very early in the year this year they reopened up their site as soon as they all felt that COVID-19.
Was better managed up there at that point.
We also did look into the impact of COVID-19 in the first half of last year, particularly in the context of renal and liver transplant and amazingly enough sites learn to mitigate the risk of organ transplant pretty quickly during spikes.
Spikes and it.
Given the precious nature of matching recipients from donors in the context of organ transplant.
Sites for the most part did very well mitigating those risks and did not really stopped performing those procedures. So I think we're anticipating the same thing heroes the vaccine rolls out.
Sites have already had an experience on how to manage COVID-19.
Last year, and I think they're doing a better job without and I think that they kind of manage that fairly effectively as far as we can tell.
Awesome. Thank you very much I'll hop back in the queue.
Your next question comes from the line of Rami Cat Caito with Lifesize capital. Please proceed with your question.
Hey, guys. Thanks for taking my questions.
I guess to start you've shown some very compelling preclinical data with HC, one and ITT can you kind of walk us through how translatable nonhuman primate model has been in transplantation.
Thanks Rami.
Let me turn that over to Steve.
I mean, what the specific question and translate ability to the clinic based on preclinical transplant data. The only data point, we have currently for blocking the pathway would be novartis molecule scallop map.
So anti CD 40, as well as anti CD 40 ligand.
Antibodies have been tested going back 30 years pre clinically in multiple species demonstrating that they can prevent both acute and long term transplant rejection, but a scalamandre.
Novartis is anti CD 40 antibody as the first.
Antibody with substantial data in renal transplant, they reported their phase II data last year, showing non inferiority to standard of care.
So that's the first.
Good sign of translate ability of blocking this pathway in the context of Oregon in cellular transplant.
Thanks, that's helpful. And then one more if you don't mind, but with regards to AOS is neuro inflammation pregnant throughout the course of disease or more so during periods of progression.
Yeah.
So unlike autoimmune diseases like lupus, where players and then holiday periods. If you want to call them that are very common and people can become fairly asymptomatic turn.
Non FLIR periods Aol's us much more progressive of a disease once symptom onset starts and so in the long run Tootle studies that have been completed nail off be inflammatory signature that we see is measurable throat disease course, and that's probably due to the fact that it's from more progressive disease.
Makes sense. Thanks again.
Yeah.
Your next question comes from the line of Thomas Smith with S V B Leerink.
Please provide your question.
Yeah.
Hey, guys. Good afternoon, thanks for taking the questions and congrats on all the progress.
Maybe you can just talk about your planned data presentation at the American transplant Congress here in June.
What are you expecting to present and what can we expect to learn about $8 51 at the conference and then secondly on the islet cell trial.
Congrats on getting the green light to resume recruitment there I know you were targeting total enrollment at around 12 patients into the study, but it is an open label trial and you've guided to taking an interim look at the data I think in the first half of 2022.
How many patients do you think you'll need for the interim and what are you looking for specifically in that analysis.
Yes.
Did you want me to take the conference question first Yeah, why don't you.
Yeah.
So I'm going to do both okay. So so we submitted four abstracts to the American transplant Congress in.
Really excited we actually got all four of them accepted.
So two of them got accepted for presentations from two of them got accepted for posters.
And so we're really going to unveil the whole history of 81, which we've never published so the first poster is going to talk about.
Dod.
Design of the antibody in vitro characterization for FC effector function than.
In vitro data to demonstrate lack of platelet activation.
And other cell based assay showing functional activity of the antibody and blocking an immune response.
So that was kind of the first part of making the antibody and making sure to have the.
Binding efficiency and everything else that we wanted in the antibody. The second poster is focused on the non human primate Tox data.
We did three different non human Primate studies, we did a PK studies just to look at quickly look at pharmacokinetics of the antibody.
In primates. The second study was a 12 week Tox study.
And then the third study was a six month 26 week Tox studies will be presenting all of that data in a second poster.
Two presentations one of them is focused on work that was done by normal Kenyon at University of Miami, It's the islet cell transplant data in her non human primate model and actually normal was going to present that data herself and then the other presentation is the presentation of all of our phase one data there was primarily in healthy.
And tears, but with one cohort of <unk> patients and I'm presenting that presentation. The Congress hasn't given up the full agenda, yet so I don't know what days and times those are.
But I heard that Theyre coming out the first week of April so either late this week or index, we should have better ideas on days from timing.
Did you want me to answer the second question that you want to take that one please go.
Go ahead.
So for the interim analysis that we're planning for next year, we think that if we can we can look at interim data with about four subjects.
With four subjects of people that are at least 90 days post transplant.
That's going to provide a lot of valuable information for us. So as you can imagine we're focusing on a patient population of type one diabetes.
Moving on exogenous insulin for a very long period of time decades.
The islet cell transplant allows us to very quickly look at islet cell function noninvasively, because we can look at C. Peptide levels. We can monitor if we get these people off of exogenous insulin with a single islet cell transplant, rather than historically with Cal sooner ahead of or is it also often takes two or three.
Transplants to get people a big enough pilots some assets survives in order to get them off exogenous and some were hoping to decrease that number and typically.
Surgeons will evaluate that at around 75 to 90 days post transplant. So we'll have a pretty good idea of not only of islet cell function. We'll know if we've gotten people off of exogenous insulin post transplant.
And then long term, we're going to be looking at other outcome measures that are really important to patient quality of life such as have we modulated the number of glycemic awareness events that people encounter over some period of time.
Looking at continued long term islet sole function.
Clearly, we're still looking at safety and Tolerability in studies like this but with four subjects, we should get a pretty good idea about islet cell function and the ability to get people off exogenous insulin.
Great. Thanks, Steve.
Thanks for taking the questions and congrats on the upcoming data presentations looking forward to that in June.
Thank you. Thank you.
Your next question comes from the line of Matt Kaplan with Ladenburg. Please proceed with your question.
Hey, guys. Good afternoon, thanks for taking the questions.
Just wanted to dig in a little bit further Steve perhaps.
You could in terms of.
You know one and how it differentiate potentially from other programs targeting CD 40, or really CD 40, like that ligand and and and how you see it.
Kind of.
Perhaps separating from us.
So Matt we look at those with two different questions. So I'm going to answer them sequentially. The first one is really what do we think the differences between targeting the ligand on the receptor.
And the second one is how do we think AG 51 might be different than the other antibodies that are out there.
Correct, Yes, exactly yes, so on the first one we think about it in a few different ways. We know based on 20 to 30 years of working on the receptor ligand pathway that they're both really critical two mediating full immune function. However, we do know that these receptors in the ligand are expressed very.
Differently in the body C. D 40 ligand has a much more restricted expression pattern. It's on platelets and go for yourselves them activated lymphocytes, whereas the receptor is much more ubiquitously expressed it's on every antigen presenting cell in your body b cells monocytes macrophages dendritic cells and every one of you.
Tissues has specialized antigen presenting cells, including your gotten your skin. So when you think about the bio distribution of antibodies that are blocking the ligand from the receptor, we're probably going to see some differences on receptor occupancy and dosing in order to block the receptor versus the ligand.
The second one biologically is that we always think that C. D 40 ligand only binds CD 40 on answers you're presenting cells to activate co stimulatory signaling and that's not true it actually binds to multiple integrant multiple different receptors on antigen presenting cells and as an example, it also binds CD love them.
So when you block C. D 40 ligand signaling you're blocking multiple different co stimulatory pathways in.
In the context of CD 11, as an example, it's really important for the activation of CDA positive cytotoxic lymphocytes in the context of acute transplant rejection. So when you block the ligand you're getting multiple different co stimulatory blocks, whereas you don't get that with the receptor.
And then the third one that's very unique to blocking CD 40 log in and that's because it's expressed on CD four positive lymphocytes. When you block C. D 40 ligand on CD four positive cells not only are you blocking their pro inflammatory differentiation you actually convert them into T Reg cells, which are <unk>.
<unk> T cells that secrete IL 10, TGF beta or another team of kinds of accretive localized tolerant genetic environment. So again. This is one of the reasons why we think blocking the ligand might be very effective compared to blocking the receptor in the context of preventing acute and long term transplant rejection.
So as far as your second does that makes sense yeah, no that's very helpful.
So as far as your second question on differentiating <unk> from some of the other antibodies. There's lots of different antibody formats that are out there if you will or I should probably call them biological formats to block the ligand.
So we went with a full antibody a T 15 don't want is a full <unk> one with point mutations from the FCC to cripple FC effector function, but elegant experiments back from the early two thousands showed that you could block C. D 40 ligand signaling without FC effector function by using F. N. B's. So just ahead of an antibody.
And then to make them have better drug like properties people pegylate them and Thats, what UCB has done with their pegylated fab that's been in the clinic for lupus.
You can work with domain antibodies, which are single train antibodies that don't have FC effector function.
<unk> is an example of that so totally antibodies, commonly made by BMS is another way to do that.
And then you can make fusion proteins. So in the case of yellow bio they made a tier three fusion protein with tier three scaffolds that have high affinity to blocking the ligand and then to give them better drug like properties.
The fuse them for things like human serum albumin to give them a better half life.
So those are the ways those are the other formats that are currently out there.
And of course, we want with a full antibody because of manufacture ability in predicting that.
Antibody has very good predictable drug like properties from the case of 81, those things have really panned out for us we have a very good robust manufacturing process with long so high yield cell line and our antibody has a half life of 18 to 26 days, which as you know.
Two to two five times longer.
Then some of the other formats that are out there.
Okay. Yeah. Thanks for the added detail and then and you you provided some details in terms of the interim look and.
Cell transplant.
How should we think about the study that you plan to initiate I guess in the middle of this year second quarter for renal transplantation and will you take an interim look there and what should we look for if you do.
Yeah. So.
The plan is to.
To try to design the studies that we'd be able to take it.
An interim look during that trial as well.
You would it for obvious reasons, we wouldn't look at the primary endpoint, but likely rely on biomarkers for that look.
But right now all of that is really.
Pending.
Ongoing regulatory discussions starting with getting the regulatory clearance to proceed.
So as soon as we have that and we begin to launch the drops will come back and provide.
Just a lot more color in terms of trial design and what to expect one.
But the goal is to.
To be able to have an interim look doing that trial as well.
Okay fair enough.
Congrats on the progress.
Yes.
Thank you.
As a reminder, if you'd like to ask a question. Please press star one on your telephone keypad as a reminder, if you'd like to ask a question. Please press star one on your telephone keypad one moment. Please while we poll for more questions.
Your next question comes from the line of Vernon Bernardino with H C. Wainwright. Please proceed with your question.
Hi, guys. Thanks for taking my question and congrats on the progress looking forward to.
The gates being opened for the set of studies to.
Advanced this year.
Most of my questions have been asked just one follow up regarding the.
Pursuit of our autoimmune nephritis indication what work still needs to be done because as you guided.
You look to initiate the phase III with <unk> one in late 2021.
So in terms of the ongoing work I think the.
The preclinical work that we've done is.
Is largely complete in terms of what we expect to need to do.
The cadence here has more to do.
With.
With our company size and being able to.
To launch trials in a way.
Where we can manage them effectively.
So we started.
With AOS, we then moved into islet cell transplant, we're now in the process of.
We're now in the process of hope.
Hopefully being able to start.
Renal transplantation and once we have that ongoing will then be able to shift our focus and resources due to the fourth indication.
Essence of the field is progressing quite quickly and we're seeing even some.
Some drugs get approved for example in lupus nephritis for the first time.
We're following those evolutions carefully as we consider.
As we consider which specific.
In sub indication autoimmune nephritis, we should focus on.
So its really has to do with the strategic decision.
Tied around the timing when we will have to make that decision.
And part of that.
<unk>.
Hi.
Requiring Jeff Bornstein till you get on board and hiring a team.
So we have a team that we've been building and we've been expanding our team.
The acquisition of analysis set.
Today, we have.
A well built out our clinical development.
And operations organization.
Jeff will definitely be an important addition to the team.
And then early thoughts you can provide as far as Oh, where Texas efforts without it.
Foundation.
Yes, so vertex which used to be acquired a company called summer.
And when they were looking to do is stem cell.
Stem cell derived islet cells. So it's while we're.
We're looking at the therapeutic approach.
So thinking about the immuno module tour immunosuppressive regimen and that needs to be given concurrently.
With islet cell grafts.
Our taxes looking at the supply of those grafts.
And working on.
Developing an approach where.
Were those cells could be manufactured as opposed to needing to come from me.
From a donor.
Okay.
Since the especially with the first generation sells those continue to need our understanding is that those continue to need immunosuppression.
The two approaches are quite complementary.
So that if a bit since any issues that may exist with us with C&I has in the past.
One may expect that they would occur again.
Even with.
With very taxes or other companies that are doing similar similar things sales.
Yes.
Perfect. Thank you truly differentiation I appreciate you taking my questions.
Ladies and gentlemen.
We have reached the end of the question and answer session and I would like to turn the call back to Doctor growth for closing remarks.
Thank you again to everyone joining us on our first quarterly call with <unk> Pharmaceuticals, we look forward to the continued advancement of our programs and to keeping you updated of our progress.
Have a great evening.
Okay.
This concludes today's conference you may disconnect your lines at this time. Thank you for your participation.
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