Q1 2021 INmune Bio Inc Earnings Call
[music].
Greetings and welcome to the immune bio first quarter, 2020 one earnings call.
At this time all participants are in a listen only mode.
The 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 and.
The reminder of 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 and co founder and Chief Financial Officer of immune bio David the floor is yours.
Thank you Doug and good afternoon, everyone. We thank you for joining us for the call of the immune Bio's first quarter 2021 financial results with me on the call is Doctor RJ test the CEO and co founder of immune bio who will provide a business update.
Before we begin I remind 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 provisions of the private Securities Litigation Reform Act of 1995 D.
These statements involve risks and uncertainties that can cause actual results to differ materially from those in such forward looking statements.
Please see the forward looking statements disclaimer on the company's earnings press release, as well as risk factors and the company the SEC filings, including our most recent quarterly filing with the SEC.
There is no assurance of any specific outcome.
Undue reliance should not be placed on forward looking statements, which speak only as of the day. They are made as of the facts and circumstances underlying these forward looking statements may change.
Except as required by law immune bio disclaims any obligations to update these forward looking statements to reflect future information events or circumstances.
Now with the forward looking statements behind us I'd like to turn the call over to Doctor RG tests, the co founder and CEO of immune bio RJ.
Thank you David and.
Thanks, everyone for joining the call idle well range my remarks to highlight the key takeaways for the first quarter and provide updates on our platform programs before I pass it back to David to discuss on financial results and upcoming milestones and we will move to Q&A.
As I did last quarter I'll begin today's call with ex folks 15, 95, which we are developing for <unk>.
Alzheimer's disease, and other CNS indications, where neuro inflammation plays an important role.
And I think recapping, our hypothesis neuro inflammation results and synaptic loss and neuro degeneration also known as nerve cell loss or death and patients with Alzheimer's disease nerve cells are where the memories of stored.
Synapses are the wires that allow the nerve cells to communicate cod.
Cognitive decline can occur when nerve cells die that as the memories of loss.
With synaptic dysfunction.
That is the nerve cells can't communicate with each other.
The combination of synaptic dysfunction, and nerve degeneration causes cognitive decline and patients with Alzheimer's disease.
We believe that for a drug to be effective in treating Alzheimer's disease and must fix one or both of these that's all that's all of the cheese based.
Based on data released so far ex pro 15 95, the drug we are developing for the treatment of the house I missed disease appears to approve improve.
The solid Gs.
Our Alzheimer's program is all about targeting and controlling neuro inflammation with ex broke 15 95, we believe neuro inflammation is a core pathology of Alzheimer's debenture that must be controlled to treat cognitive decline.
On the 23rd of January we reported data on nine patients who had completed the full 12 week treatment period with EXPAREL three.
And three in the low dose group and six and the high dose group of one milligram per kilogram once a week of the subcutaneous injection.
We've expanded the data presented and from that we had presented in July of 2020 to provide additional insight into the effects of exports. If the 95 and these patients with the eight Alzheimer's disease I will focus on four highlights of that presentation.
We demonstrated a highly significant correlation between measures of white matter of free water using MRI.
With inflammatory cytokines and the CSF obtained by the lumbar puncture.
Ex pro caused both measures to decrease substantially and significantly suggesting that white matter of free water may be a non invasive measure of neuro inflammation that will spare patients the need for and the base of lumbar puncture of the sample.
The S F and CSF the cerebral spinal fluid.
The CSF proteome day that provides hence to the benefits of controlling neuro inflammation with Expo hi.
Highly significant decreases and neuro filament, one and visit like protein one both biomarkers of nerve degeneration suggests nerve cell death.
Is decreased.
Significant increase and synaptic proteins connect and too.
And now are granted and demonstrate improve synaptic function.
We presented the example of CNS remodeling and a patient who over nine months of weekly ex float treatment had improvements and impair of fiber density a novel measure of white matter of quality and improvements and critical disarray measurements and novel measure of grey matter of quality.
Although we only showed one patient this result was not unique.
Eight of the nine patients reported in January were stable.
Or showed improved cognition over the three months period.
And the patients who responded with the greatest decrease and neuro inflammation had the greatest improvements and measures of their cognitive performance.
During those three months of note.
We.
Dented, the scans of white and gray matter of quality and a patient.
And that.
Presentation. This patient was unique and because we had the scan but he had to quit his will retire from his work because its debenture was progressive after six months of Exco therapy. He was able to return to work.
We continue to fall of these patients who are on the extension study and intend to provide further updates and the progress I would encourage you to review the K O L. Webinar from the January 21st present.
The presentation. It is available on our website on.
Also all of what I've talked about is available on the slide format and on.
Non confidential corporate slide deck also found on our website.
We find these results compelling they clearly demonstrate that the treatment of ex broke 15 95, when given as a once a week subcutaneous injection for at least three months and patients with neuro inflammation with Alzheimer's disease have a decrease and that neuro inflammation. We remained committed to starting a blinded randomized placebo.
Well controlled study by the end of the year.
And the meantime, we continue to generate data and our phase one trial and and the patients who opted to stay on ex pro and the extension study as a reminder, the duration of the phase. One study is three months. The patients can then at the joined and extension study that allows an additional nine months of therapy.
A handful of patients who have been on ex pro for year one.
When we report additional data from the phase one the summer we will provide data from new patients and the three months study additional biomarker data and all patients give insight into those who remain who receive long term ex pro therapy and the extension study.
And provide details of the phase two trial design and needless to say based on our results to date, we are very excited about the future of this program.
A remarkable attribute of ex broke 15 95 is that the ability to control neuro inflammation and really cuts across a large range of neuro degenerative and psychiatric diseases, where neuro inflammation.
As a core of pathology.
What do I mean by that if you're developing a drug that targets. The amyloid you can really only treat.
Alzheimer's disease.
With ex Pro 15, 95, we can treat any CNS disease, where neuro inflammation plays an important role so that gives us a much.
The bigger operating field a current example is.
On the is to use ex pro 15, 95 for the treatment for treatment resistant depression. This phase II trial and supported by a $2 9 million grant from from.
From the small business innovation research.
The administration associated with the NIH and we will receive that money over the length of the phase III trial.
The treatment resistant depression market is substantial and the U S and estimated 7 million patients suffered from T. R D.
The current treatment paradigm involves a trial and error of cycling through therapies find one that works. The patient is label treatment resistance. Once they have failed two regimens this hit and Miss approaches frustrating from patients and the clinical team and increase the cost of care and that cost is.
Substantial it is estimated that the cost of treatment resistant depression exceed $64 billion of year to the U S health care system.
There is a real need for therapeutic advancements.
As with the a D trial, we will use biomarkers of inflammation to confirm.
And that treatment resistance is likely due to neuro inflammation. Once the diagnosis is confirmed patients are enrolled treated for six weeks. The determined response the extra therapy the.
Use of Biomarkers is not routine and psychiatric drug development. We believe a precision medicine approach will make development of new drugs for depression, more efficient and will provide more effective therapies.
We will conduct this trial in collaboration with two of the world's pioneers of the field Professor Andy Miller and Associate Professor Jim Feld, you both of Emory University and.
The six week trial will be of double blind placebo controlled study of ex pro versus placebo 45 patients per arm.
Biomarkers of inflammation will be measured at baseline two and six weeks. The primary endpoint is improved functional kick connectivity measured by MRI.
And reduction of Biomarkers of inflammation secondary endpoints include clinical measures of motivation, which is the most.
Sensitive measure of and patients with treatment resistant depression, we are on track to begin this trial later this year.
[laughter] Queller is the name of the drug we used to treat patients and our COVID-19 program that targets. The cytokine storm the patients hospitalized with respiratory compromise due to COVID-19, the double blind randomized placebo controlled trial is designed to enroll 366 high risk COVID-19 pay.
<unk> and two equal sized cohorts one cohort is the placebo plus standard of care, while the other this color plus standard of care of the primary endpoint is the need for mechanical ventilation or death during the 28 days following enrollment and the study.
The secondary endpoints include transfer to the ICU Neulasta net of neurologic cardiovascular thromboembolic or renal disease.
The sum of the data safety monitoring board will who will give us a go no go decision after evaluating the data and the first group of patients if they go it is.
Is given the trial will proceed and ultimately 366 patients will be in low.
And commune is our and cat and K cell priming platform as you know NK cells are part of the innate immune system the play a crucial and.
And increasingly important role in cancer outcomes. They have the bar of ability, it's target both active disease, and particularly target residual disease, which is the cause of cancer relapse and fact.
Yeah.
T cells are not the play very little of any role and clearing residual disease that is the target is the cause of relapse and patients with cancer.
This has been a frustrating trial to get off the ground because of the many months of COVID-19 related delays across the UK, but we are screening patients.
And for treatment and the phase one trial of including in patients with high risk Myelodysplastic syndrome or high risk Mds.
High risk Mds is the serious hematologic and hemo poetic stem cell disorder in which patients have functionally the effective NK cells and this allows there.
The blast or their marrow to be overtaken with glass, which prevents which causes progressive and of the disease and ultimately decrease of survival approximately one third of the M. D. S cases progressed and bell.
Current treatments include chemotherapy and bone marrow with stem cell transplantation, but these patients are all of their elderly and they just many of them are not candidates for chemotherapy or aggressive.
And transplantation strategies, so a M.
Immuno therapy makes sense.
And this trial, we hope the show that by delivering.
A therapy that primes NK cells that therapy, zinc and the patient's own NK cells and I emphasize their own NK cells can be reprogrammed to kill the tumor. This open label study will enroll nine patients and the dose escalation strategy.
All of these patients will have Mds with ex us less the primary endpoint of safety and Tolerability of Tolerability of income and when administered IV secondary endpoints include the change and the number and percentage of glass overall response rate, which is really hematologic measures and these patients.
And also using the W. H O criteria and the dessert duration of that response.
We have the opportunity to expand the trial, it's really easily moved into a phase III. If the results are attractive.
We recently put a short five minute video up on our website and it does a really wonderful job of explaining.
Why NK cells felt the clear cancer.
And now the cellular and molecular interactions.
By Intermune.
With the patient's own NK cells activate them to kill resistant tumors.
This another way the patient.
Most patients had plenty of NK cells and those NK cells have all the as I like to say guns, and knives and missiles to kill cancer, but they need they need to be.
Crime, they need a trigger to get them going after that cancer and commune provides that trigger.
As I said the video can be found on our website and we hope you take a look at it.
Finally.
As we indicated last quarter and Theres been no change and B O. Three are promising oncology program has been delayed due to COVID-19, we hope to initiate the phase two trial and muck for positive cancer. Once the pandemic is better control. Although this program is clinically dorman.
<unk> research on the combination of M. D L. Three with tyrosine kinase inhibitors and <unk> four expressing tumors continue.
Really we have not initiated the phase two trial in Nash and this will not occur until the pandemic has been completely controlled.
We hope to have more clarity on these programs once the future.
Of the pandemic is better understood.
I'll now turn.
The the floor back to David Moss, our CFO to discuss the financial results and upcoming announcements.
Thank you RJ I'll provide a brief overview of our financial results and upcoming milestones and net loss attributable to common stockholders for the quarter ended March 31, 2021 was approximately $4 6 million compared to approximately two point million for the comparable period in 2020.
Research and development expenses totaled approximately $2 5 million for the quarter ended March 31, 2021 compared with approximately.
800000 for the comparable period in 2020.
The primary reason for the increase and expense was an increase in R&D activities related to our clinical programs and costs associated with manufacturing and additional drug supply.
General and administrative expenses was approximately $2 1 million for the quarter ended March 31st 2021, compared to $1 3 million for the comparable period in 2020.
At March 31, 2021, the company had cash and cash equivalents of approximately $45 3 million with no debt.
The cash includes net proceeds of approximately $28 4 million that we raised through our ATM facility.
During the three months ending March 31 2021.
As of May five 2021, the company had approximately $14 9 million shares of common stock outstanding.
Now I'd like to move on enlist our upcoming milestones and catalysts.
As argued had pointed out earlier this summer we will provide a go no go decision by the data safety monitoring board. Following the first group of patients treated regarding the continuation of our quality of trial for the treatment of pulmonary complications from COVID-19.
Towards the end of this year, we plan to initiate our phase two all timers disease program with extra $50 95, and patients with neuro inflammation.
We'll provide more clarity on the design of this program, including the estimated cost and time line of the phase two trial as we get closer to this milestone.
Also towards the end of the year, we plan to initiate a phase II trial of ex Pro 15, 95 and patients with treatment resistant depression and was partially funded by a $2 9 million of NIH Grant that we should receive over the length of the phase II trial.
Furthermore, the.
It's RJ mentioned earlier, we're currently screening patients for Eaton and study and high risk Mds and we'll report further information as of this trial moves forward.
In addition, assuming the clinical landscape has not changed we are planning trials and our other programs. Once the COVID-19 pandemic has been controlled and our trial sites give us. The go ahead. These include live and eight phase two for the treatment of Nash in the O phase two for the treatment of muck for resistant.
Metastatic her two positive breast cancer.
So in summary, notwithstanding the pandemic, we believe we're making very good progress, particularly on our neuro inflammatory franchise. Following the compelling expanded Alzheimer's disease data that we reported in January.
At this point I'd like to thank you very much for your time and attention and I'd like to turn it back to the operator, Doug to poll for questions Doug.
Ladies and gentlemen at this time, we would be conducting a question and answer session. If you'd like to ask a question you May press star one on your telephone keypad, a confirmation tone will indicate your line is in the question queue. You May Press Star two if you would like to remove your question from the Q4 participants using speaker equipment and it may be necessary to pick up your handset.
Before pressing the starkey.
Our first question comes from the line of Jonathan Aschoff with Roth Capital Partners. Please proceed with your question.
Thank you Archie can you tell us what biomarker data, we can expect to see and the final phase one Alzheimer's date of release and if the FDA favors and specific markers.
Okay. Thank you Jonathan.
Remember the purpose of that trial is to is really twofold. One is to help us define which biomarkers to use.
Use of patient selection and our phase II trial, and two to really use shall we say indirect measures or or provide and indirect evidence of the biology of improvements and the bank. So when I talk about biomarkers and I'm talking about things like.
White matter of free water of parent fiber density.
Looking at.
CRP and the blood those of Biomarkers of inflammation and of improvement.
Of cortical tissue.
The FDA quite frankly doesn't yet care about these they have made it abundantly clear that the only approvable endpoints.
For Alzheimer's disease relate to Cogs improvements and cognition using some choice of a panel of of analytics that are well established and the literature. So you know to be blunt. The F. D. A doesn't care what biomarkers, we want to use they're going to be looking at.
Those cognitive endpoints, which will be part of the.
Endpoints and the phase II trial, our Biomarkers help us pick the patience of pick the dose pick the duration designed the study to hopefully prevent us from having a study of this not conclusive.
So.
You know I just use this think about of biomarker that is used for encore.
Oncology.
The bio mall of biomarker can either be used to help with the drug development patient selection et cetera or be used as a validated surrogate biomarker for efficacy progression free survival is of Great example of a validated surrogate endpoint, although it doesn't predict overall so.
Rival the F D a six.
Acceptance to my knowledge there are no.
Validated surrogate endpoints and Alzheimer's disease, so for our phase two and beyond trials, we will always use cognition as an important endpoint because at the end of the day as it stands now that's the only thing you can get approved for.
With the FDA and outside of.
That answer your question Jonathan.
Absolutely. Thank you very much of a J, that's all of that I had.
Our next.
Question coming from the line of me and my Tommy with B Riley Securities. Please proceed with your question.
Hi, good afternoon, and thanks for taking my question and congrats on the progress. So in terms of just following up on the previous question on the upcoming extra data disclosure.
And Oh Gee could you clarify how many patients you may have on the low and high dose and and.
Also on the fee, while the update that biomarker would.
Would you have more patients that you could report more data on that and and then I have a follow up on the phase.
Phase two study design.
Yeah. Thank you.
And where we anticipate having 17 minimum maybe as many as as is.
18 or 20 excuse.
And excuse me is 24 and for that data analysis.
But what's important and we really have two categories of data and I'm glad you gave me the chance to talk about this remember I stated that the primary trial goes three months.
So we'll have white matter of free water on all of those patients will also have some of our more interesting biomarkers like the parents fiber density and critical.
Disarray measures on those patients, but as the patients get rolled over and do the extension trial.
They still get Biomarkers, not CSF, but they get you know bloods and MRI scans at six nine and 12 months, so not the full cohort, but many of the patients that have reached.
Six nine or 12 months, we will have scans on those as well as you know cognitive testing and this will of safety laboratories, and all of that so we will be able to expand the amount of information that we are able to give not only expand the number of patients.
But we'd be able to expand the length of the therapy and one of the things I really want to reemphasize is that at three months all of the patients had CSF protium draw on the CSF Proteome is this incredible warehouse of information I mean, there was something like 37000 of proteins we've owned.
And when.
It did.
A small number of those we continue to mine that data and quite frankly, it's pretty interesting stuff, but the bottom line is from the perspective of U S and the Investor we will be talking about more patients. We were talking about patients who have been followed for up to a year.
And that set of data will be we will put into the sausage maker, so to speak and and one of the primary path that we will do and the August release will be give you very clear guidance on what the phase II looks like you know who the patients are going to be what the duration.
And what the dose et cetera, because we will be starting at the soon after that and as you know the phase two blinded placebo controlled trial is really what makes or breaks of this program.
Right. Thank you.
And that was very helpful and then on the phase two design.
RJ.
Are there any biomarkers here that the B M on the Ibs.
And any of that you feel could have prognostic value, where you could have and enrichment strategy for maybe identifying the law.
The responders and and maybe following that through any of the longer term kind of study I'm just curious you know.
Since you are seeing some movement and these biomarker led a very short time Peter.
So great question and so as you know when we designed the trial really the focus on neuro inflammation and we selected.
Patients, who had and had either you know and elevated CRP elevated sound rate elevate the hemoglobin day, one see or where April.
Four of positive.
And based on our analytics. The date, we you know to the credit of of C.
C J born of moves the head of our neuroscience programs I think we got it right. We did a good job selecting those patients right because those patients all had neuro inflammation by both CSF cytokines, which is what you're used to seeing and by the white matter of free water. So we're pretty comfortable with our patient selection.
We have some of the <unk>.
Intrigued with some biomarkers that May show.
Evidence of early response and.
And we will be talking more about that and August we're not yet ready to go public, but I will say on equivocally that our biomarker strategy is paying dividends.
You know some of that is you just got lucky when you're doing something novel like this you have to make some informed guesses.
No our informed guesses are turning out to be pretty good and we will provide all of that data going forward.
But just think about you know just think as white and out of free water is being the little bit of a tip of an iceberg here because theres a lot and.
There'll be more interesting stuff coming behind and I and I hate to leave you hanging, but you kind of have to wait the August yeah.
Great and just and my final question was on.
And if anything like this any insight on the biomarker work you may also do and PID and.
And if theres any read through from the loans, you've done and now it's Amazon J D.
Yeah. So good question you know the the biomarker, we're using is of functional MRI scan that's very specific for.
And for treatment resistant depression. This is work out of by Miller and sells your from a from the.
University from Emory University, we will be using all of our other tricks that.
And that we've been deploying and the Alzheimer's trials and these patients.
Remember I said during the discussion and one of the beauties of ex pro is the we target neuro inflammation neuro inflammation cuts across a lot of different diseases, and the CNS space, both neuro degenerative disease and psychiatric diseases. So the the things we learned on Alzheimer's, we can apply to treatment resistant.
Depression, the things, we learn and treatment resistant depression, and Alzheimer's weekend, we can apply to the next disease. The thing we apply and learn in the first three big cities and we can apply to the fourth disease. So it's really there are no kind of one offs. Here. This is what is pretty exciting and of and I gave the example.
All of the Targa.
Targeting amyloid with and anti amyloid drug I mean, once you get back get done with Alzheimer's disease, you have nothing to do with that drug now.
That's a good place to be if you have and effective drug but in our case we.
We will not only be we think very effective for each individual disease, but the fact is we can play this card over and over again of course.
I can give you a long list of of diseases, but just go look at our website look at the publications and you could make a list of of 10 or 12 different diseases that will be attacking with the single drug.
Great and looking forward to more updates thank you Archie.
Our next question comes from the line of Jason Mccarthy with Maxim Group. Please proceed with your question.
Hey, guys. Thanks for taking the questions just kind of building a little bit more on the Alzheimers disease, given all the activity, we've seen more and the last one.
On a 12 months or so around inflammatory biomarkers and use of Biomarkers and.
And to advance to later stage trials is the next stage two <unk>.
Brad I'm going to have.
Call. It 30 to 50 patients, maybe a little bit more with the three months biomarker.
And point that you can look at and say I have of drug here will continue on.
With the cognition stuff out of 12 months, maybe six nine and 12 months that we can start designing a phase III around what we're seeing here, we did see it once before this year.
And we're wondering if that's something that you're thinking about or how youre thinking about it.
[laughter] them on Jason the other thing like putting me on the slide here I love It and.
No.
You're barking up the right tree year, basically we believe the Biomarkers will allow us to make sure we're headed and the right direction.
I think it's a little bit early to say.
You know.
That well because we see what's happening at three months, we know what's going to be happening and 12 months at least I don't I don't think we can do that with you know the the small number of patients. We have we may have more patients under our belt I think we will be able to make that conclusion. There is a precedent and Alzheimer's disease for three months data and not.
Being consistent with you know a little bit longer term data, but that's and one one category of drugs. The bottom line is you're exactly correct and I've you've heard me say this before we are working very hard to avoid having to do and 18 months trial.
We think of an 18 month trial might be relevant and amyloid anti amyloid strategies it might be relevant in and.
Anti Tau strategies, but we think the reason that's relevant parents, because you are taking and indirect approach to actually treating the disease. If you take a more direct approach, which we believe Expo is targeting the information. We don't believe you need the wait that long and I predict although I'm not yet ready to.
To give an exact number but I predict that we will our phase two will be significantly shorter than 18 months and will provide us with all of the quality of data we need now our goal is a little different than what you articulated you articulated that we wanted to take a look at three months no. If we have a drug on.
Our goal is after the end of the phase two to have enough insight that when we pick the patient enrollment criteria for the phase III, we basically know we pick the group of patients where we're going to bring the belt right and in fact, you know so far we you know we know that we have like I.
Said earlier, we did have the the very simple biomarkers, we chose for enrollment criteria did a very good job of enriching for patients with neuro inflammation.
And now we have more tools to work with so we're going to get even better.
Got it and and on the treatment resistant depression side.
And as the program going to have measures of depression, and a lot of matter of scores pick your flavor of number of matter score.
And that's one question and then in terms of.
Prioritizing.
And mental health related diseases like tier D. How do you look at it through the lens of what's coming down the road with all of the psychedelic based company and piling into the treatment resistant depression, because its happening now and theres going to be a lot more.
NASDAQ listings and the next six to 12 months and it's going to be right in the window of when you start. This trial is that something that you're considering as well.
So so that's that's good so that's the that's a good question. So yes, we are definitely measuring all of the other measures of depression, the anhedonia motivation.
Motivation I meant I called the motivation and the and the and the tax is really the primary.
Clinical endpoint and we use that turns out to be a very difficult treatment and a very common symptom and patients with treatment resistant depression.
The psychedelics is an interesting question. The question is is this a bubble you know one of those the the.
The new shiny ball on Wall Street or is you know what is the they're there and I think time will tell.
I think the use of the so I could tell you now I'm on.
And I'm, a child of the sixties man and I remember I remember of different use of psychedelic but I think it's fascinating.
They are being repurposed to treat these difficult disease and so I think time will tell I am very confident we have the site is and that is doing the <unk> study of we have it at Emory.
Emory and at our UA D. These are the investigators who are very interested and the role of TNF and this disease I am confident that we'll be able to enroll the small number of patients. If we reach the point that we need to do of 500 patient trial. After this.
And then competition with the with drug development and the psychedelics may be problematic, but for now.
I think that you know.
I continue to watch this with interest like you do.
That's right and my point was not compare like you said shiny ball on Wall Street that was my point and not competing against them, but more of do you.
Become more T. R D facing in terms of prioritizing it as a public company because of what happened sometimes of these shiny ball on Wall Street like Nash, we thought might be you know all of the story.
That was my question also yeah, well that's a you know we we've been pretty clear about our strategies.
We have followed the science.
More than we've followed the.
On the.
The Investor interest I think you know the COVID-19 is the is the exception there. We followed what we felt was a you know the right thing to do as a company and the space during the dark days of of March 2020 you remember that the when New York was just about the fall off the map with COVID-19.
And 19.
But for the most part we pretty much fall of the science and we fall of who gives US. The money you know why are we in Alzheimer's disease because of the Alzheimer's Association gave us of millions of dollars.
Why are we and the T R D because the.
And I H gave us almost $3 million, so you know where.
And then you know are we we're opportunists.
But we also have a drug that we can play and various spaces and even if you gave us the money, we're not going to go there unless the science of sound our science of sound.
Got it thank you RJ.
Our next question comes from the line of Thomas Shrader with BT argue. Please proceed with your question.
Hi, guys.
Does it somehow and putting in for Tom first of all and thank you for the update and taking my question. So kind of building off the biomarker for the extra on 15 95 for your ongoing pace. The one trial for Alzheimer.
I was wondering if we should expect any additional imaging biomarker data beyond the white matter of free water for the future of retail.
Definitely and we are very excited about these you know we've been working with two vendors and Micah and Oxford brain diagnostics and.
<unk> is our white matter analytics group and Oxford brain diagnostics is our gray matter group I mean, we will definitely have.
Data on more patients and.
Right and that of free water of more patients so increase breath, but increased depth and the white matter in particular, because there are of biomarkers that we only hinted that.
Previously from for instance of parent fiber density, which turned out to be quite interesting, but I will say that we need to do some more work and we're working closely with them because of all the time on this and you will hear more about it but I think I think the bottom line is that.
CNS drug development is changing with these new tools that we have on our fingertips. We're gonna do we meaning the biotech community is going to do a better job of developing drugs and the CNS space and I think we the new bio have been leaders and this I think we're ahead of everyone and we hope the.
<unk> of that every time, we get to talk to you and present new data.
And that's exciting thank you.
Okay.
Our next question comes from the line of Michael Erwin with Universe Security. Please proceed with your question.
Alright, guys.
And there's been recently and we've seen the business downturn do you think there's the <unk>.
P O E. Four gene has some things to alzheimers.
Formation, causing damages and active.
And can that with me and for early detection isn't the gene of interest from research and development for export of 15 95 moving forward.
Oh Oh.
So.
Yeah. At this point you know we used April E. Four which is a gene for one of our inclusion criteria is interestingly in the United States of lot of people know what their April we force status is and as you know it is enriched and patients.
And with Alzheimer's disease.
I think we are yet convinced of other.
Jean Jean the approaches at this point, but.
But I would say that we are all always have an open mind I mean, obviously the beauty of of of.
The genetic markers as they're relatively easy to get.
But at this point, we do not have plans beyond April four.
But as.
The day, the changes not only what's available to us, but on our own data changes that may change.
Okay.
And also of the husband some research around the counter drug sorry go on most.
And for the Repurposing for all kinds of drugs to create more white blood cells and diseases and they have and thank you so on something.
Promising data and or through trial and what are your opinions on the mis approaches and white blood cells and B perhaps.
For the kinds of growth.
So if I understand your question there are attempts to improve whites.
Basically.
White blood cell, where macrophage function as a way to treat Alzheimer's disease.
So I'm not going to comment on those but I will say unequivocally we agree with the hypothesis that.
And part of.
The problem with at least the Alzheimer's is the microglia function dysfunction.
Which and micro glial cells, our branch of the White blood cell you know family.
Is the cause of the disease, because they lose their ability to phagocytose debris, particularly and.
Amyloid debris. So the principle is correct we believe that.
And that improving phagocytic function.
We'll help cleaned out the garbage of the brain and if you clean out the garbage of the brain youre going to have a better effect on.
On your ability to treat diseases.
What I think is interesting and Jason kind of mentioned it a little bit is how suddenly you're seeing a lot of new therapeutic strategies come out of the woodwork since in the last year or two I mean, five four of five years ago. I mean, we were we were of Lonely voice and the Alzheimer's space. Besides really for all practical purposes by.
And that has.
Changed and I think it reflects the increased.
Optimism.
And by the Biopharma and Investor community that you know we.
We may have a chance with Alzheimer's, particularly if you know the FDA Green lights.
And a can of mab from Biogen. This this June so we're excited you know at this point, we're like anybody who wants to come join the party. That's fine but you know this is a hard disease, it's a hard disease, the crack and but.
We're going to do it.
Okay. Thank you.
Our next question comes from the line of Daniel Carlson with <unk> Research. Please proceed with your question.
Hey, guys.
Jay question for you about neuro inflammation and as it relates to on COVID-19 and I'm wondering if you guys are going to be doing anything and this and anytime soon.
Well as you know we're careful about talking about our strategic plans until we're really ready to talk about them, but we have been following the law on COVID-19 story very carefully.
And obviously, it's a appears to be a very big problem. It appears to be of problem without a lot of hypotheses.
What is causing it.
Obviously, we think neuro and flame formation plays an important role, although I have to say the data on.
The thin the data the symptoms looked like neuro inflammation, but the clinical correlation has been thin to date.
We are very closely following the space, Dan and given <unk>.
Once we get one.
Enough data and ideally too.
And the government the NIH steps up with some funding streams. This is obviously and option for.
The <unk>.
For ex pro if we can be convinced and others, including the NIH and would do the funding.
That neuro inflammation plays an important role.
Yeah.
Got you and then if I could just ask one other question.
Since the since it looks like.
The successful you'll be treating all of the samaras patients for a very long time I'm. Just wondering if you have any any additional long term safety data.
As it is ex broke continued to be safe for the patients are on it from 12 18 months and then also along those lines of you're looking at any other delivery methodologies besides injection.
Yeah, yes, the both I mean, you know we have as I said, we have a handful of patients out of 12 months they remain on the drug.
Have remained on the drug for 12 months and that's as much data as we've had so far and I can tell you that no. One has stopped the drug after three months because of of of.
Safety issues, just think of the current TNF inhibitors remember this is a better TNF inhibitor and the current TNF inhibitors people are on those for many many years. So I am we are have always felt that the risk of of this drug development program failing because of safety was going to be low.
So compared to some other types of drugs that you might treat.
Other delivery strategies are pretty interesting ideas, we do and although we break that into two areas. Obviously, there's delivery strategies to allow us to go after different diseases that becomes kind of the shall we say a.
A.
And the technique to expand the usefulness of the drug and the other one is to determine whether to decide and make it easier to give the patients quite honestly.
Patients have been pretty.
Comfortable with a once a week sub Q injection and it's not like you're of diabetic where you're having to give yourself five injections a day or.
Two injections a day. This is once a week with a 26 gauge needle it's a it's and our hope is that it will be a.
One of these.
Self injectors the people use like on Epipen that is very well tolerated. So you know our I have to say those we talk about that but our main focus currently.
And is to make sure we get the phase III trial design right.
Because if the trade to trial design.
It doesn't do what we expect it to do we could have all of the formulations and delivery systems, and we want but they're not going to be very useful.
Yeah, and I'm looking forward to seeing that design and and the other phase one results. So thank you.
There are no further questions and the queue I'd like to hand, the call back to the Doctor testing for closing remarks.
Well. Thank you all for quite a long call. This was almost 90 minutes and I. Appreciate you, allowing me the stand on my Soapbox, but part of that is because I think we are very excited about the ex pro program and Alzheimer's disease. I think you can sense that from the way we present the data and I. Thank you.
Should be able the sense and increasing confidence and our.
And our program as we go for it and a lot of that is due to the credit of the team led by.
C J Barnum likewise, the COVID-19 and inked and programs are coming along we believe our future is bright.
Thank you for your interest and I can't wait till we get to see you all face to face again.
Thank you very much.
Ladies and gentlemen, this does conclude today's teleconference. Thank you for your participation you may disconnect. Your lines at this time and have a wonderful day.