Q3 2021 INmune Bio Inc Earnings Call
Greetings and welcome to the immune <unk> third quarter 2021 earnings 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. As a reminder, this conference is being recorded a transcript will follow within 24 hours of this conference call. At this time. It is my pleasure to introduce Mr. David Moss co founder and CFO of immune bio David the floor.
As yours.
Thank you Hector and good afternoon, everybody. We thank you for joining us for the call for immune <unk> third quarter 2021 financial results with me on the call is Doctor RJ Tassie, CEO and cofounder of <unk>, who will provide a business update on our DN TNF platform and Dr. Mark Labelle CFO.
So and co founder who will provide an update on our NK cell priming platform.
We're also lucky to have doctors CJ Barnum head of neuroscience, who will speak about our newly announced phase III program in mild cognitive impairment or NCI.
Before we begin.
Mine, everyone that except for statements of historical facts. The statements made by management and responses to questions. On this conference call are forward looking statements under the Safe Harbor provision of the private Securities Litigation Reform Act of 1995.
These statements involve risks and uncertainties that could cause.
Actual results to differ materially from those.
But forward looking statements.
Please see the forward looking statement disclaimer in the company's earnings press release as well as the risk factors in the company's SEC filings, including our most recently quarterly filings with the SEC.
There is no assurance of any specific outcome.
Due reliance should not be placed on forward looking statements, which speak only as of the date. They are made and then stuff the facts and circumstances underlying forward looking statements may change.
Except as required by law in mobile displays any obligation to update these forward looking statements to reflect Q3 for me that's worked perfectly.
Now I'd like to turn the call over to Dr. RJ.
Co founder and CEO of the new body armor.
Hey.
Thank you David and thank everyone for joining the call as is our practice I will arrange my remarks to highlight the key takeaways from the third quarter and subsequent period and provide updates on our platform programs I will start by reviewing our DN TNF programs, then hand the call.
Two CJ Barnum head of neuroscience for immune bio who will speak about our new phase two program in patients with Mci.
Which is a prodromal form of.
Alzheimer's disease Professor Mark with Dell, our CSO will speak about recent developments with the encomium platform before I pass it back to David Moss.
Our CFO to discuss the financial results and upcoming milestones then we'll move to Q&A.
Exco is our CNS platform, we have clinical programs in Alzheimer's disease, and treatment resistant depression with R&D, enabling studies underway and a L. S.
Each of these programs are supported by extra Merle non dilutive funding from the Alzheimer's Association, the NIH and the AOS Foundation, respectively.
The common denominator denominator of the CNS indications is that neuro inflammation plays an important role in the disease neuro inflammation. However is one step removed from the true pathology underlying Alzheimer's disease.
Those changes are loss of connections between neurons and nerve cell death in the brain neurons have two parks sell body is in the gray matter and the myelinated axons or in the white matter. The first is where the memories are stored the ladder allows neurons to communicate both.
Our required for normal cognitive function.
Inflammation causes synaptic dysfunction strips axons of their mylan and drives neuro degeneration of both axons in nerve cells.
Put simply neuro inflammation dramatically alters grain biology, precluding normal function.
Immune buyer believes the synaptic connections can be restored and myelinated axons can be repaired with X pro therapy immune bio's using novel technology to demonstrate the importance of white matter pathology in Alzheimer's disease.
MRI biomarkers of white matter free water apparent fiber density and radio density.
Measures of neuro inflammation axonal integrity in myelination, respectively help locate and quantify waiting out a pathology then measure the effect of <unk> therapy.
These powerful technologies provide new opportunities for staging and treatment of <unk>.
CNS diseases and highlight the many effects of EXPAREL therapy the.
The opportunities to use X pro beyond Alzheimer's disease or a real.
More than 60 publications covering more than a dozen diseases gives us into the opportunities before us.
These publications can be found on our website.
We've given three webinars discussing the results from the phase one study of X pro in Alzheimer's disease patients. So summarized treatment with EXPAREL for three months decreases neuro inflammation decreases neuro degeneration and promote improves synaptic function in patients with Alzheimer's disease.
The last two benefits of expert to target therapy that is the core pathology of cognitive decline, which is X pro which is nerve cell death and synaptic dysfunction.
In our opinion, if a drug for a D does not improve one or both of these variables theres a little hope that the drug will make a difference in cognition.
Our data show that X pro improves both and does much more.
During the third quarter, we released additional biomarker data that further supports our belief that extra will make a difference in patients with Alzheimer's disease.
Much of the new biomarker data is focused on white matter of pathology.
Extra improves multiple measures of white matter pathology. Unlike traditional volumetric analysis of the brain advances in MRI imaging allows us to measure the microstructural changes of specific white matter tracks as well as actions and Mylan within the white matter track.
Using techniques called the parents fiber density and radial diffusivity respectively.
The concept of white matter tracks, maybe new deal white matter tracks or axonal superhighways to connects parts of the brain that must work together there are many white matter tracks, but and not all are important in Alzheimer's disease. Our analysis is focused on the so called seven a D whiting out of bundle.
Those are the bunch of white matter tracks, most affected by Alzheimer's disease and they include names like you know the anterior fasciculus the front of our occipital.
Corpus callosum cingulum just to name a few.
The phase one trial had two steps all patients were treated for three months and six patients retrieved X pro for up to a year in the so-called extension trial in the patients treated for 12 months was X pro in the extension trial, there was continuous improvement in white matter volumetric changes in the temp.
Willow and increases in the parents fiber density and radial diffusivity within the a D bundles of 17 and 16% respectively.
You may be thinking that doesn't sound like much but it is to give perspective over a 12 month period apparent fiber density and radio diffuse diffusivity get worse in patients with Alzheimer's disease to our knowledge improvement in these metrics has never been seen in patients.
<unk>.
These observations are these improvements are supported by data from the CSF protium.
That will be presented next week at sea tab, which is the big clinical trials, Alzheimer's disease, meaning occurring in Boston.
We also observed an effect on X pro our more traditional biomarkers of disease, specifically Tao.
That was a structural protein necessary for Exxon integrity, when phosphorylated the axon degenerate.
Phosphorylated Tau proteins are liberated from dying axons and can be detected in the CSF. The more phosphorylated Tau present more white matter loss is occurring.
Of the many tau species phosphate to 17 has the highest discriminative accuracy for Alzheimer's disease, and a strong correlation with amyloidosis and cognitive decline.
When assessed and are patients treated with ex pro for three months. She has slipped CSF levels of phosphorus tell 217 decreased 46%.
In summary, extra improves the biology of brains in patients with Alzheimer's disease. It decreases biomarkers of neuro inflammation in neuro degeneration, while improving biomarkers of synaptic function myelination in white matter brain volume.
Our phase one trial like nearly all phase one trials is without a placebo arm. What is missing is the effect on cognition. We've told the story of the patient who quit work because of this dimension and then after six months of extra therapy return to his position as an educator educator, we love that story, but I understand it is anan.
Nick Dote.
The phase two trial is a blinded randomized placebo controlled trial designed to allow us to determine if six months of extra therapy in patients with mild they D.
We will have an impact on cognition, we believe it will and like you. We look forward to the results of the trial.
We have previously announced the design of the phase two trial of EXPAREL in patients with mild a D and biomarkers of inflammation, we call. This a D. I, that's a capital a capital D small lie Alzheimer's disease with inflammation.
While the Adi is defined as a clinical dementia rating of <unk> or C. D. R. <unk>, five and one or one and they have biomarkers of information that are required for enrollment.
The six month trial will enroll 201 patients the primary cognitive endpoint will be E. Mac early a D slash Mci Alzheimer's cognitive composite.
There'll be multiple secondary endpoints in both cognition function and biology with MRI.
Although we are the first to use the Mac as a primary endpoint in the Alzheimer's disease trial, we will not be the only wants to do so Dr. Judy Yeager of Albert Einstein College of Medicine, a recognized expert in the measurement of cognition will deliver a talk at the upcoming <unk> meeting next week detailing the advantages of <unk>.
Mac over the currently used primary endpoints in clinical trials.
To encourage participation in the trial.
Now to help recruit patients quite frankly, we have set up a randomization of two to one so of those 201 patients two thirds will get drug.
Those are complete a six month treatment will be eligible for 12, a 12 months instinct expend a lot extension trial and we will continue to collect data on those patients during the extension trial.
Placebo patients will be allowed to switchover to the X pro therapy.
Many have asked how we can conduct a phase II Alzheimer's trial that small 201 patients in short six months. The answer lies in our biomarker driven development strategy, which aims to choose patients that progress quickly and have a low variability in the rate of progression.
These are elements that provide a statistical advantage and trial design.
The details of how these calculations will be were made will be presented at <unk> next week.
We intend anticipate 40 trial sites to be opened in the U S, Canada, and Australia because of a biomarker.
Based inclusion criteria, we predict there'll be a 50% screen failure rate.
This combined with the renewed enthusiasm towards a D drug development falling the attic can't imagine approval means increased competition for patients, we expect enrollment which will start.
This quarter will be achieved at a measured pace, we do not anticipate reporting top line data until the second half of 2023, we will try to beat that but that is our current predictions.
Today, we announced the phase II trial, using X pro to treat patients with Mci and a biomarker of inflammation. We believe the early.
The earlier the disease is treated more like E. Lee progression can be stopped with the hope of reversing the disease and keeping it away.
In a moment CJ Barnum the head of neuroscience is for immune vial will give more details on the trial.
Well I started in M C I trial now.
The answer is simple.
We watch with interest the rush of companies seeking approval for anti amyloid therapies based on phase II trials using the F. D. A accelerated approval mechanisms commonly used to gain conditional approval in oncology.
It is too early to know exactly how this will play out for exco, but we are preparing for accelerated approval. After successful completion of our phase II programs two elements are necessary for success clinically relevant efficacy data and an ample safety database.
We believe the potential weakness of a single trial strategy is not enough safety data.
Adding a second phase two it has the potential to expand both the efficacy and the safety databases C. J.
Thank you RJ.
Our second phase two study will be an mci patients with information, which we refer to as a D O three.
This will be a three month 90 patient randomized placebo controlled study with endpoints of biological and cognitive biomarkers.
Patients will be assigned to one of three treatment groups placebo, one meg per kg or to make per keg of EXPAREL.
As in the mild a D study, which we now referred to as a D. O. Two the primary endpoint will be the E Mac.
Secondary clinical endpoints will include the Cogs state cognitive battery.
D. R goal attainment scale, the NPI and activities of daily living.
Dairy biological endpoints include imaging, MRI, neuro inflammation, and white matter blood and CSF to measure inflammatory and Neurodegenerative biomarkers and functional Biomarkers E G and speech and language analysis.
We believe the latter two biomarkers will provide important functional data on the impact of the biological changes we see in the brain after treatment with EXPAREL.
E G will be assessed using a portable E. G platform developed by Cumulus neuroscience that we'll collect E. G data from the comfort of the patients' home.
We determined feasibility of this platform on a subset of patients in the phase one study.
Beach and language analysis has also been shown to be a sensitive biomarker for disease and holds promise as a biomarker for treatment response. The addition of EG in speech analysis provides a functional biological readout that will further enrich our understanding of the biological response to EXPAREL.
At the end of the three month study all patients, including those randomized to placebo will be eligible to enroll in a 12 month extension study, where all patients will receive EXPAREL and.
And both phase two studies the extension trials will increase the quality of the safety database needed for our approval strategy.
Why do we choose three months.
Despite mci and early mild patients often being lumped together as early a D and clinical trials biologically. They are not the same as an example, white matter changes presents differently and in different brain regions. There is also evidence that inflammation is not the same in M C.
I in 80 patients in other words, the biomarkers that were so informative and mild 80 patients in our phase one study might not be relevant for Mci patients. This study will identify the appropriate biomarkers for Mci patients, while also assessing the potential clinical benefit for EXPAREL.
We are confident that this study will provide the information necessary to further our understanding of Mci. Thank you everyone back to Ya Orchard.
Thank you C J.
Like to emphasize that X pro has many uses in the treatment of CNS diseases, you've heard me say, it's not a one trick pony.
We've announced a phase II trial of Expo in treatment resistant depression. This trial is supported in part by a $2 $9 million grant from the NIH consistent with our a D development strategy, we will select patients with biomarkers of inflammation and.
And measure functional activity of a pathway in the brain tied to both treatment resistant depression and inflammation using MRI.
As with Alzheimer's disease, the enrichment strategy and target engagement for the treatment resistant.
Depression patients with neuro inflammation in lines with the pathology of the disease excuse me aligns the pathology of the disease with a mechanism of action of EXPAREL.
This is a six week double blind placebo controlled study of T. R. D patients. The primary outcome measure is the functional activity connectivity measured by MRI, but we will also measure change in biomarkers of inflammation and improvement and more traditional clinical measures.
We have dubbed Inkerman, our natural killer cell platform, a suite of kind of what is a suitor cline well in commune is not an NK cell. We don't give NK cells. It is not a cytokines, we don't give where you cytokines in any part of the ink immune therapy.
Binds to the patients NK cells in vivo.
And does the NK cells, what it takes a cocktail of cytokines to do ex vivo.
That is you know in a test tube.
That cocktail of cytokines includes IL 12, IL 15, and IL 18.
Importantly.
NK cells produced by ink noon or memory like NK cells. The NK cells that are better at killing cancer cells.
The first patient was treated in our phase one trial evaluating aikman and Mds high.
High risk Myelodysplastic syndrome. It is a serious hematopoietic cell disorder that can transform to AML professor Mark with Dell co founder and CSO of the company and quite frankly, the inventor of the whole intermune kind of hypothesis will provide information on the status of it.
Our incoming program Mark.
Thank you Andre and thank you everyone for listening. So that's all the trade said 2021 has seen the opening of our first clinical trial, we think need after considerable delays, we suffered because of the COVID-19 pandemic.
The first in human trial.
She was a single center in the U K I mean, it's enrolling patients as Andre said with the bone marrow disease called monitor dysplastic syndrome.
The trial is a dose escalation trial typical a nice phase ones with three dose cohorts.
The first patient was treated at the lowest dose and received three of those low doses over a two week period.
We would have liked it to C. D showed no adverse reactions to any of the infusions, but most importantly, he showed an almost immediate response strychnine with systemic activation of his peripheral blood NK cells and the development of NK cells in the blood with a memory like phenotype, which should enhance tumor killing in the laboratory analysis.
Right the way through to his most recent test on day 73 place treatment and CFO. He's completed over 100 days of follow up and remains well.
In fact, the day 119 samples where in the lab to diet of being tested presently and we hope to find that he retains activation of NK cells and his peripheral blood with that ability to kill a.
Tumor cells better.
We will continue to monitor him, but at present, having spoken to his position today is disease appears to be controlled and he reports to these quality of life has improved.
A long kind of COVID-19 in the U K, however, still restricts enrollment of cancer patients into trials are they reluctant to come into hospital since they fear.
Section.
So to increase recruitment we are applying to open a second trial in the U K to the U K medicines regulator.
Now in discussion with a third well.
We're also looking at trials overseas.
So in the coming weeks, we will submit an application to the U K as mentioned regulates to the M. A X ray to open a second trial with <unk> in ovarian cancer, which had been our plans for our original trial and we anticipate trial commencement in the first half of 2022, a gain in a single central initially in the U K.
Most recently, we were also supply Inc. Being on a compassionate basis to treat the young Lady under the age of 20, who suffered acute myeloid leukemia.
And he had relapsed after receiving a transplant from an unrelated volunteer donor.
And she developed chemotherapy resistant acute myeloid leukemia.
She received a slightly higher dosing clean than the M. D. S trial patient, but again over three consecutive two consecutive weeks three consecutive doses she.
She to show no adverse events to the treatment, which was encouraging given it was three times the dose.
And her blood counts have improved so much that she's being discharged from hospital for the first time in seven months and is now at home.
She's waiting a second stem cell transplant is a curative option and possibly associated with that future, Inc, including treatment to consolidate the transplant.
It's important to remember that this young Lady was not treated within the clinical trial and that's drawing conclusions about the efficacy would be inappropriate.
The condition treating her beliefs that she's better than Cumulus before he came in therapy and she certainly no longer neutropenia.
Which is allowed to be discharged goodbye.
So early phase clinical trials in cancer remained challenging in the U K and elsewhere in the post Covid era, and we're now seeking trials in the U S mainland Europe to expand the Mds trial program.
Meanwhile, My lab in the U K continues to investigate the biology, I think activation by clean and the improvement of cancer targeting and our preclinical research program a much of these data were presented at the British Society for Immunology Conference in December whether you beat it by 6%.
I'll now pass the call back to Jay Thank you very much.
Thank you Mark.
Everyone knows a lot more about COVID-19 today than we did two years ago mortality rate has fallen 10 fold from 20% in March 2022% today, all hospitalized patients receive corticosteroids and rest of the Cherry and respiratory therapies is much more sophisticated today than at the beginning of the pen.
Mike vaccination vaccination, and soon and anti viral pills and maybe even in an inexpensive oral psychiatric treatment are changing the need for hospitalization.
Out of our successful biomarker strategy and Alzheimer's disease, the virtual biopsy using M. R. I allows us to quantify white matter of pathology and we believe our phase two trials will correlate improvements in those biomarkers with improvements in cognition.
I believe we are entering the Golden age of C. N S drug development and immune by I was leading the effort to use powerful new tools to move C. N S programs forward.
Companies like ours are always thinking validation from the academic world. The form for this validation is peer reviewed medical meetings.
A few days ago, we announced five abstracts accepted at the upcoming 14th clinical trials.
Upcoming see tab meeting, which is being held in Boston next week to our oral presentations, one including the one on E. Mac cognitive M point I referenced early earlier three are in the three posters have a common theme that studying white matter of pathology allows us to quantify disease burden and pay.
<unk> with Alzheimer's disease, and measure response to therapy, we believe our success. It see Tad reflects an interest in the novel techniques, we bring to the field.
At this point I'll turn the call back over to David Moss or CFO to review certain financial terms.
Thank you R. J I'll provide a brief overview of our financial results in upcoming milestones before we head to the Q&A session.
Net loss attributable to common stockholders for the quarter ended September 30th 2021 was approximately 9.5 million compared with approximately 4.7 million the comparable period in 2020 <unk>.
Research and development expenses total approximately 6.5 million for the quarter ended September 30th 2021, compared with approximately $2.4 million for the comparable period in 2020.
Primary reason for the increase in expense was an increase in R&D activities related to a clinical programs and costs associated with manufacturing additional drug supply.
General and administrative expenses was approximately 2.5 million for the quarter ended September 30th 2021, compared to 2.5 million the comparable period in 2020.
As of September 30th 2021, the company had cash and cash equivalents of approximately 84.5 million.
Based on our current operating plan, we believe our cash is sufficient to thunder operations into 2023.
As of November 3rd 2021, the company had approximately 17.8 billion shares of common stock outstanding.
Now I'd like to move on and lift our upcoming milestones.
In the fourth quarter, we plant initiate our faith to program for mild all timer's disease with expert in patients with Neuroinflammation.
Barring any competitive or pandemic related delays, we expect this trial to have top one results in the second half of 2023.
And the first half of 2022, we plan to initiate a fee three months 90 patient as to program.
For mild cognitive impairment similarly, barring any unexpected delays, we anticipate having topline results in the first half of 2023.
Also shortly after the start of the H a D program, we plan to initiate a phase two trial of X pro in patients with treatment resistant depression that is partially funded by a $2.9 million.
N I M H screen.
We expect further open label high risk inpatient data as the program continues to angle and finally, we plan to launch a second Aikman study in a very cancer in the first half of 2022.
Since summary, we're pleased with their progress during the third quarter as we continue to advance our too piper or two platforms towards potentially value creating milestones.
At this point Hector I would liked it well at this point I'd like to thank you for your time and attention and I'd like to turn it back to the operator to pull for questions Hector.
Thank you at this time will be conducting a question and answer session. If you'd like to ask a question. Please press star one on your telephone keypad, a confirmation code to indicate your line is in a question Q you May press start to if you'd like to remove your question from the queue for participants using speaker equipment and may be necessary to pick up your handset before pressing.
Darkies one moment, please while we pull for questions [laughter].
[noise] [noise] [noise]. Our first question comes from line of Tom Schrader with B T. I D. Please proceed with your question [laughter]. Good afternoon, congratulations on the progress [laughter] So I.
Wanted to ask a little bit about E. Mack how how experimental that is if I understood. It works earlier than eight us cog, but if you get patients kind of on the borderline of mild a D and M. C. I does it does it say the same thing as a highly correlated.
C J.
Yeah. So great question. So the answer is the Iraq was empirically derived and early M. C. I and early mild a D. So it works extremely well for both groups and the reason for that is because the E. Mac is.
Is measuring cognitive symptoms that are relevant.
For does our cognitive disease progression and that card.
[noise] Yeah. Thomas This is Tom this if I can jump in here I mean, I really encourage you to try to listen to Judy Yeager's talk it seeped out if not we can arrange for her to call you, but I mean basically she developed this with industry players because people.
I have not been satisfied with a D. S. Cog in these and these mild you know a D. N M. C. I patients. It's just very atheist caused the C. D are just very blunt instrument. So this should give more sensitive evaluation of their cognition and.
Apparently allows us to tell if they are remaining stable or even improving and as you've heard me say I think that actually that is the industry's belief that decreasing and the rate of decline is a.
I consider a low hurdle and we have higher aspirations for the way Expo will work.
[noise] [noise] yeah secondhand.
Okay sorry.
Yeah, one more thing as it relates to the regulatory pathway. So you'll hear from Judy that we're not the only ones that are using EMACS. There are other if you go to clinical trials I called other companies are using the metric and we believe we have all the boxes checked off that the F. D a requires to be.
To use a novel metric for a primary endpoint. So we think we are well positioned in that'd be angle.
Okay I have a couple of questions on inclusion criteria your inflammatory markers. So for instance, H b a one scene. That's barely pre diabetes is is that where inflammation is already full blown and then a second question is your choosing not to use plaque is.
Inclusion criteria I understand your view of the role in Ah pathology, but it's a pretty good way to make sure you have all simers patients. If you remember some of the early Solon as a matter of trial. They think a third of the patients didn't have all farmers. So just your thoughts as his diagnosis without plaque better now.
No.
First of all to be clear Yeah go ahead C J.
Yeah, Let me answer the second one first so we are requiring the patient to be amyloid positive okay I'm sorry.
Yeah, no. That's a that's a request I mean, they're very clear that Alzheimer's patients have plaque full stuff. Okay got it got it got it.
Okay.
And then now hemoglobin, a one C. Yeah hemoglobin, a one C. I think is <unk> <unk>.
Very insightful biomarker by and Nubile for two reasons one they have these patients do have inflammation peripheral information to remember you've all heard me say for years, the peripheral information begets Central information. The other thing is you know there is an important ellen.
<unk> of of of insulin resistance.
And that can cause dementia right now people forget that back when we were doing Nash that one of the findings was that Expo actually decreases insulin resistance alright. So in fact, I think we're gonna <unk> I think there's a potential for a double whammy year that not only do we have an impact on.
Inflammation and hemoglobin, a one C does select patients who have neuroinflammation, you'll see more of that information that <unk>.
But importantly, you may be getting to fertilize, we like to say, we may actually be having a secondary effect on those chubby patients who have peripheral inflammation and dementia due to their amyloid due to Alzheimer's disease. So.
Alright, great. Thanks.
As a reminder, if you'd like to ask a question. Please press star one on your telephone keypad now as a reminder, if you'd like to ask a question. Please press star one on your telephone keypad now one moment, please while we pull for more questions.
Next question comes from one of my ankle and I'm tiny with be Riley. Please proceed with your question.
Hey, this is William on from out of my money I really appreciate you taking or accuse a few quick ones from US first off could you provide some additional color on what investors should be focused on it she tied presentations and what we might be expecting there could be new.
[noise] well you saw the press release I think from last week and you know I think.
As far there's I would say you know we will they'll be more information on how.
Shall we say reliable white matter free water M R I'm metrics or in the disease and measuring the disease pathology in therapy, you'll see data on increased additional data on the CSF protium.
And how what affects X pro has on it and then I think the the EMACS story as we've mentioned a couple of times will be clarified I think it's important I think one of the things that that management has been frustrated at by quite honestly as we you know we are.
I think we've been on the cutting edge of using novel.
Biomarkers, but I think that and we don't this is not a criticism rightfully so investors a little bit uncomfortable because these are biomarkers that a lot of other companies aren't using now we think they will be using them soon.
But it is our responsibility to make sure the investment community and the academic community understand how important these biomarkers are into diagnosing and staging the disease and looking for therapeutic response. So I think there's gonna be you know the the new stuff is.
Gonna be relatively incremental there's no there's not gonna be any you know.
Knock you off the off your socks kind of stuff, but it's gonna give you a lot more why hope we hope. It gives you more confidence that we are playing in a sandbox that nobody else is playing in that in fact, we have Ah. We're what we're doing makes sense and we believe that more and more patients will be using.
The kind of Biomarkers that we are using for their future trials because.
They work pretty well.
Awesome really appreciate that and then also you had mentioned for your X prone T. R. D that you're gonna be using a similar enrichment arm microstrategy like you did in a D. I was curious if we could get some any extra information on what those biomarkers or American strategy might be.
<unk> yeah yeah.
Yeah. So so you know there really incredible thing about depression feel this.
C. R P. As a biomarker for treatment response with anti T N. After like because it's.
As well established it's been shown in and multiple clinical trials and we have evidence from that with in patients with chronic.
Chronic neuro inflammatory diseases like rheumatoid arthritis smell. So so CRP. We've got we've got a really good biomarker was CRP, that's well established but we've actually added to that a little bit we ever be we've added a behavioral biomarker of Antonia. So it turns out that one of the most prominent symptoms associated with information.
And is reflected within the the region of the brain that were looking for functional connectivity is antonia. So when we combine those two things together, we've got both the behavior on a biological biomarker that help us in rich further the patients that are most likely to respond.
Gotcha, and then real quickly.
Are you or can can we expect any type of in terminalis shoes for either your 80 trials safety check or anything like that in between the initiation into topline.
No. Unfortunately, it is a a very pure blinded randomized trial, so because it's only six months and we know six months of therapy as well tolerated in these patients. There is no you know safe.
There's always safety announced but there's no potential those to stop the trial unless you know something terribly important happens. So we think that you know that's why we like a six month trial remember almost everybody else is 18 months trials. So I'm looking for something halfway through make some sense cause you're looking at for something that.
Nine months, we'll have our results before them.
Alright. Thank you makes me a lot of sense I really appreciate you taking my questions congratulations on everything.
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 R. J Tessie for closing remarks.
[noise]. So thank you we continue to make progress on both our platform programs remain confident that are are indepth understanding of the science and the mechanism of action and the use of Biomarkers will lead to efficient development strategies, we will aggressively pursue accelerated approval strategies for our.
<unk> disease program, we do not know if we will be eligible for or successful in those efforts, but you ignore them would not be fair to patients or our shareholders.
Finally, I remind you that you're only seeing the opportunities at the tip of the iceberg for each platform.
There are many opportunities yet to be presented has resources grow our efforts will expand and you'll see what those other opportunities look like with that we thank you for participating in.
In the call.
And I'm sure we'll be speaking to some of you over the next couple of weeks.
Ladies and gentlemen. This concludes today's conference you may disconnect. Your lines at this time. Thank you all for your participation.
[noise] [music].