Q4 2020 INmune Bio Inc Earnings Call
[music].
Greetings and welcome to the immune bio of fourth quarter 2020 earnings Conference call.
At this time all participants are in a listen only mode. A question and answer session will follow the formal presentation.
If anyone should require operator assistance during the conference. Please press star zero on your telephone keypad.
As a reminder of this conference call is being recorded.
The 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 is yours.
Thank you Rob and good afternoon, everybody. We thank you for joining us for the call for immune Bio's fourth quarter 2020 financial results.
With me on the call is Doctor RJ, Tessie, CEO and co founder of immune bio who will provide a business update.
Before we begin I'll remind everybody that except for forward 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 <unk>.
<unk> 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 from the company's 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.
Sept as required by law <unk> bio disclaims any obligation to update these forward looking statements to reflect future information events or circumstances.
With the forward looking statements behind US now I'd like to turn the call over to Doctor RJ test the co founder and CEO of the new bio RJ.
Thank you David and thank you everyone for joining the call I'll arrange my remarks to highlight the key takeaways for the fourth quarter.
Year to date and provide updates of.
On our platform programs before I pass it back to David to discuss our financial results and upcoming milestones and then we will move to Q&A I'll.
I'll start with our DN TNF platform, beginning with X Pro 59, which we're developing for Alzheimer's disease, and other CNS indications, where neuro inflammation plays an important role.
The clear highlights since our last quarterly update was data we reported on January 21st from our Phase one trial of <unk> in patients with Alzheimer's disease.
<unk> bio is data driven hypothesis is that neuro inflammation results from synaptic loss and nerds of generation that is nerve cell death in patients with Alzheimer's disease synaptic loss and narrowed the generation is the cause of called cognitive decline in these unfortunate patients.
Finally, we believe the control of neuro inflammation by export of 15 95.
We'll help for repair synaptic dysfunction decreased neuro degeneration and prevent progression of cognitive decline.
Last July we announced interim data demonstrating the <unk> $15 95, reduce neuro inflammation by an average of 40% and the argument fasciculus.
The white matter of track the important for learning and memory in patients with Alzheimer's disease.
No inflammation was assessed using MRI to measure white matter of free water, a validated biomarker of neuro inflammation.
The small preliminary data set included six patients three of the low and high dose group.
Treated with ex pro for 12 weeks as a reminder of the phase one trial is the neuro inflammation trial in patients with Alzheimer's disease.
At that time based on the quality of the data we committed to initiating a phase II clinical trial in Alzheimer's disease by the end of 'twenty 'twenty, one we remain committed to that goal.
On January of 'twenty for first we provided additional data from nine patients who had completed the 12 week treatment period with X Pro $15 95. The group included the original three patients who received weekly subcutaneous injections of <unk> three milligram per kilogram of Expro 15 95.
Hi.
And now six patients who received one milligram per kilogram.
Once a week these are the low and high dose groups respectively.
We wanted to accomplish two goals with the date of release in January 1st we wanted to connect the dots between white matter of free water measured by MRI.
Uh huh.
A validated but new biomarker of neuro inflammation with traditional biomarkers of neuro inflammation, namely CSF cytokines. The second goal was to determine if the downstream consequences of decreasing neuro inflammation in the small group of intensively studied patients.
<unk> what was seen in the extents of animal data using X from models of neuro degeneration.
To accomplish the first goal we use the <unk> platform.
Two of two measure of 47 of inflammatory chemo kinds and cytokine levels in the CSF of patients CSF by the way as cerebral spinal fluid that is obtained by lumbar puncture.
But to measure of those levels in the CSS of patients before and after three months of Expo 15 95 therapy.
The cytokines all decreased significantly for example, CCL two excuse me CCL seven it came of kind of the really mirrors, what happens with soluble TNF decreased by 47%. After 12 weeks of X Pro therapy and you can see this in the slide.
The decrease in the white matter of free water and the decrease in the inflammatory chemo kinds in cytokines correlated closely on the next slide and you can see that the R. Squared value is greater than 7.7, which is a highly statistically significant correlation.
Despite a small number of patients what this means for the future is that the MRI using MRI to measure of white matter of free water at least when looking at neuro inflammation may be able to replace.
CSF in lumbar puncture.
That's what the future of holds.
The results presented so far have really met the primary goal of the phase. One study that is to demonstrate the <unk> Pro 15, 95 decreases neuro inflammation in patients with Alzheimer's disease.
We've clearly shown this now on for the second question. The second question is what are the downstream consequences of decreasing their own formation in patients with Alzheimer's disease, we used to biomarker platforms to provide insights into the consequences of the decreasing neuro inflammation the firm.
First was proteome Biosciences TMT calibrated the study the changes in the CSF proteome in the Alzheimer's patients before and after 12 weeks of Expro therapy. This is the big data analysis of the CSF proteome that revealed that decreasing neuro inflammation.
<unk> led to a significant change in multiple alzheimer disease related pathways, including the immune inflammatory response pathway the.
The sea us CNS neurons function and injury pathway.
And the dendritic spine more for Jeff morphogenesis synaptic clusters.
The plasticity pathway.
Notably the analysis found a 80 per cent decrease in neuro degeneration markers, such as neuro filament light chain and visit like protein, one and significant changes and connect them too narrow of granted.
Both proteins associated with neuroplasticity.
To get the drug approved in Alzheimer's disease, you must demonstrate the treatment decreases the rate of cognitive decline compared to placebo.
This trial does not attempt to really meet those standards as the primary endpoint. It's a small open label dose escalation trial, but there is important information included in the dataset the.
The data, albeit polymer preliminary and nine patients.
The only one patient had progression of their disease during the three months study.
Put another way eight of nine patients were stable or had improved cognition over the three months period.
Finally.
Six of the patients all in the high dose group.
Have been enrolled in the nine month extension study that is.
That is they basically were allowed to continue the study for nine there.
Treatment for nine months after they met had finished three months on study.
These patients received safety labs cognitive testing MRI scans every three months.
Three patients have already had a year of therapy in two of these have been approved for a special access program by the Australian government to allow the continued treatment of their Alzheimer's disease with X pro $15 95.
We continue the study these patients and you will hear more about them in the future.
In summary, the short trial in a small number of patients clearly shows that X Pro 90, 515, 95 quickly decreases neuro inflammation, resulting in positive changes in the CSF protein protium and.
In MRI scans using very sophisticated measures that you will see an example of if you go back to the Kols webinar all of this correlates with what we've seen in animal models.
We remain committed to starting a blinded randomized placebo controlled phase two clinical trial in the second half of the year.
We have a bit more work to do before we released the precise precise design of the phase II trial and.
And we continue to enroll patients in the ongoing phase one trial and continue to mine. The extensive data set that we have and are generating.
What we have learned and are learning from these patients will prove invaluable as we design the best possible phase III trial for the development of Expro, 15, 95, and Alzheimer's disease.
The second CNS trial, we plan to initiate this year isn't the treatment resistant depression or <unk> in September we announced that we were awarded a large up to a $2 $9 million grant from the <unk>.
From SB IR grant from the NIH to support a phase III trial of <unk> 90 in patient 95 in patients with treatment resistant depression.
We will conduct this trial in collaboration with two of the world's pioneers in the field Professor Andy Miller.
And associate Professor of Gen Felger, both at Emory University Dr.
Dr. Miller is the pioneer and the role of neuro inflammation in depression.
Having described the problem in the early days of NSA of interferon therapy for cancer.
And then going onto the published the first study demonstrating the targeting TNF and.
Improves depressive symptoms in patients with elevated biomarkers of inflammation.
In addition, Dr. <unk> discovered that the connectivity between two measures of the brain as measured by MRI that of vital for the feelings of pleasure in motivation our losses.
In depressed patients within from formation all.
The hypothesis is once again simple.
<unk> 15, 95 will decrease neuro inflammation.
<unk> clinical symptoms and restore connectivity between these vital regions of the brain as measured by clinical criteria and by MRI.
PRD is treatment resistant depression is a neuro inflammation program that leverages a lot of what we're learning during the phase one trial in Alzheimer's disease as with the day trial of the <unk> trial, we use biomarkers of information to confirm diagnosis enroll patients.
And determine response to X pro therapy the.
For the use of Biomarkers as a novel approach to psychiatric drug development. We believe the use of Biomarkers will improve the efficiency of drug development in the field.
And we believe we will lead that revolution.
Premium resistant depression remains an area of significant unmet need in the U S. An estimated 7 million patients.
With the major depressive disorder of resistant to current therapies.
Most often defined as having failed two prior lines of treatment.
Current treatment steri strategies required treatment resistant patients to cycle through multiple multiple therapies in an attempt to find one that works.
We hope to introduce precision into the diagnosis and treatment selection by using biomarkers to identify patients and track their progress.
These two programs highlight a key advantage of the extra $50 95 platform extra.
The extra decreases neuro inflammation neuro inflammation as the key pathology of across a number of neuro degenerative and psychiatric diseases. A quick review of more than of the more than 60 publications on our website. We will give you an idea of the breadth of the opportunity for extra of $15 95 in the CNS.
All of our Alzheimer's disease, and treatment resistant depression, or the first but not the last of our programs in CNS.
Turning now to <unk>, our COVID-19 program for.
For treating cytokine storm.
Last quarter, we went into some detail on how the cytokine storm Lance many COVID-19 patients in the hospital on why we believe targeting soluble TNF.
Is the master cytokine is potentially more effective.
More effective approach of suppressing the dis regulated immune response.
In November we announced.
That's the first patient had been rolled in the phase II trial.
Of Queller for the treatment of pulmonary complications of COVID-19.
The double blind randomized placebo controlled trial will enroll 366 high risk COVID-19 patients in two equal sized cohorts.
One cohort is the placebo of the standard of care cohort. The other is standard of care plus queller there'll be given of one milligram per kilogram subcutaneous injection of enrollment.
Second dose of color, maybe given a week later of the patient remains hospital lives.
The primary study endpoint that I'll remind you that this trial was written with the FDA, they really dictate of the design and the endpoints of the trial.
Primary endpoint is the.
The need for mechanical ventilation during the 28 days following the admission to the hospital and enrollment for the study.
Secondary endpoints include things like transfer to the ICU, new onset of neurologic cardiovascular of thromboembolic.
The renal disease and death.
The first 100 patients.
Randomized into the study will inform a go no go decision by the data safety monitoring board.
If the <unk> recommended the trial continue the remaining 266 patients will be enrolled.
We hope to reach that go no go decision by the end of second quarter.
Yeah.
Yeah.
Turning now to income you are NK cell priming platform NK cells ourselves of the innate immune system that play a crucial role in the cancer outcomes given their ability to target residual disease the cause of cancer relapse.
Hey, restores the function of the patient's own NK cells to attack the residual disease.
We believe that by eliminating residual disease, and can and should improve survival in cancer patients.
This year, we plan to initiate a single center phase I trial in the high risk Mds patients.
<unk> plastic syndrome.
Great.
Precursor to acute myeloid leukemia, the primarily effects.
Although the patients the trial is set to run in the U K.
The U K like the rest of.
The World, where we would do clinical development has had restrictions on the startup of new clinical studies.
Because of the strains.
Of the pandemic on their health care system.
We are ready to enroll patients when the NHS the National Health service, which is the UK health system gives us the green light we will initiate the trial that will include at least nine patients with the opportunity to expand both the number of centers and the number of patients.
Finally, we have previously previously announced that <unk> three our oncology program.
Has been delayed due to COVID-19, we hope to initiate the phase II trial in much for positive cancer. Once the pandemic has been control.
This program is clinically dormant laboratory research on the combination of MB of three with tyrosine kinase inhibitors and mark for expressing tumors continues.
All are Lee.
Eliminate program for Nash will not begin a phase two until the pandemic has completely control we hope to have more clarity on these programs. Once we have returned immunity in the U S and the danger of these various viral variance is understood.
I will now turn it back to David Moss.
<unk> CSO CFO to discuss the financial results.
In upcoming announcements David.
Thank you RJ I'll provide a brief overview of our financial results and upcoming milestones net.
The net loss attributable to common stockholders for the year ended December 31, 2020 was approximately $12 1 million compared to approximately $7 7 million for the year.
Year ended December 31, 2019.
Research and development expenses totaled approximately $5 9 million for the year ended December 31, 2020, and compared with approximately $3 3 million for the year ended December 31 2019 the.
The primary reason for the increase of expenses was an increase in R&D activities related to our clinical programs and costs associated with manufacturing additional drug supply.
General and administrative expense was approximately $6 3 million for the year ended December 31, 2020 compared to $6 million for the year ended December 31 2019.
At December 31, 2020, the company had cash and cash equivalents of approximately 22 million with no debt.
Sub debt subsequent to the end of the quarter. We raised gross proceeds of approximately $28 4 million through our at the market or ATM facility and issued 1 million 439480 shares of common stock.
At a price of $20.17.
Based on our current operating plan, we believe our cash is sufficient to fund our operations and achieve potentially value, creating milestones into late 2022.
As of March 4th 2021 of 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.
This current year, we plan to initiate a phase II trial of X Pro $15 95 in treatment resistant depression that is partially funded by a $2 9 million NIH grant.
We also plan to report additional data on our phase <unk> Alzheimers disease program price.
Prior to the phase two program initiating.
We also towards the end of the year plan to initiate a phase two program for Alzheimers disease with X pro $15 95 in patients with neuro inflammation.
We will provide more clarity on the design of this program, including the cost of the phase II trial as we get closer to this milestone.
In addition, assuming the clinical landscape has not changed we are planning trials in our other programs. Once COVID-19. The COVID-19 pandemic has been controlled and our trial sites give us the go ahead.
This include the income being phase one program for <unk> for high risk Mds and ovarian cancer.
Livni phase III program for the treatment of Nash.
In view of three phase two for the treatment of Mark for resistant metastatic her two positive breast cancer.
So in summary, notwithstanding the pandemic, we believe we are making good progress, particularly in our neuro inflammation franchise. Following the compelling expanded alzheimers disease data that we reported in January.
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 for Q&A.
Rob could you please poll for questions.
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. The confirmation tone will indicate your line is in the question queue. You May press star two if you'd like to remove your question from the queue for.
For participants using speaker equipment, it may be necessary the pickup your handset before pressing the star keys, one moment, please while we poll for questions.
Our first question comes from Tom Shrader with <unk>. Please proceed with your question.
Hi, good afternoon, thanks for the update.
Just the.
The phase one B trial will we see more patients or will this be deeper analyses on patients followed for more time.
Yes, Thanks, Tom Youre going to see both.
I think I've made it clear that we are exploring additional doses.
And we so we will have more patients and we will also the patients that have been studied will have longer time, so youre going to get both more doses and longer time.
Okay, and then hopefully this isn't too big of question, but for tier of D. How how do we think about this is this a subset of patients with systemic inflammation.
All patients.
And just a little bit of a sense of is there any hints as to the time of course of helping these patients and if they have T. R. D from inflammation are they reversible or would this be of stabilization I know that's like 80 question.
So I'm going to give you.
The way, we think about it we clearly think that as the subset of patients with treatment resistant disease. If you look at the Biomarkers. We used we think about a third of those TRT patients probably of Biomarkers of inflammation. That's the group we're going to focus on initially you remember we.
We do our CNS trials kind of like an oncology trial, we look for those biomarkers, it's not to say that those other patients wouldn't benefit but at this time, we don't have any data the support that so in those patients that have biomarkers of inflammation the day.
Data. We have suggests you will see a response in three months basically probably actually shorter but the trials are designed to last three months because that's what the initial data shows now I think the more interesting million dollar question is do these patients them remain on X pro or just this reset them.
So they now become responsible to let's.
Let's say, an SSRI or something like that we don't know the answer to that we do know that when patients are enrolled we don't we don't we will not be taking them off their current therapy. So they will be ended up on double therapy or a combination therapy.
And then it will be up to their clinician to the side at the end of the study just like we do in Alzheimer's, whether we'll be keeping them on X pro is kind of the compassionate use or actually it will be stopped but I think thats.
That's the second question that we need to answer. The first question is our hypothesis as clear that patients with treatment resistant disease.
Who have biomarkers of inflammation will have a will respond to therapy. If you get rid of that neuro inflammation and thats what <unk> all about.
Got it alright. Thank you that's very helpful.
Our next.
<unk> comes from Jonathan Aschoff with Roth Capital Partners. Please proceed with your question.
Thank you guys. So I was wondering if you were looking at any different neuro inflammation biomarkers for T. R D versus what Youre doing now for a day.
Yeah, Thanks, well.
As we mentioned there is this.
Special connectivity biomarker that you can see using functional MRI in the TRT patients. So that is a unique biomarker to that patient population we will be.
Measuring all of our standard MRI Biomarkers as you know we're interested in both white and gray matter markers of both inflammation and quality such as.
Critical disarray measurements will be measuring them also but those are secondary exploratory endpoints for the most part what's driving the <unk> program will be.
Really standard clinical measures using validated clinical scales of depression, and really in Indonesia, but also this very unique observation using fmri of connectivity that's associated with symptoms in these patients.
Okay. Thanks last question is I was wondering if to.
To what extent have you had inbound interest from investigators wanting to use your anti TNF.
Vacations for which you are not planning trials.
So we have a significant.
Effort that is at the preclinical stage.
In other words people ask us all the time can I get the drug. The study this model of nerve degeneration or that model, we have a very extensive and carefully.
Curated program that then we harvest the best of the best of these data and I can tell you. There's a number of programs that you have not heard about yet that we have not announced that are very promising for now on the clinical front. Our focus is really on the programs we've announced.
We believe that the CNS franchise is.
And neuro inflammation is making progress in Alzheimer's disease, and we think that will bring significant value creation.
And then allow us to expand into some of these other really unmet needs that we have on tap.
Thank you Archie.
Our next question comes from the way up of Cool Rama Caf with H C. Wainwright. Please proceed with your question.
Thank you. This is all came from Pennsylvania.
Couple of quick questions.
<unk>.
On the.
Oh on the Alzheimer's disease.
The program.
What additional data should we expect from you know from the phase one b.
And also.
You were talking.
You're talking about initiating a phase III program of newer information in the patients.
What sort of timeframe of when you're thinking off.
Yes, thanks, Okay. So.
We are as I've mentioned publicly we're exploring doses in between.
The current cohorts of point of <unk> three in one milligram per kilogram.
We see there are there is a dose response between those two groups.
As it relates to both.
Measuring white matter of free water and also looking at the CSF proteome.
So I'm not convinced we have nailed the dose so to speak so we're exploring that the reason that we're spending time, even though there's no safety signal that there is no reason that we can't use the one milligram per kilogram per week dose.
The average Alzheimer's patients survive seven years without therapy, we expect.
Patients who have therapy to be on you know have extended survival. So we can see the patient will be on drug for let's say 10 years and so we want to nail the dose because that makes a difference and as you know once you do a registration trial I mean, it's very hard to change to change the dose. So we wanted to.
We have the right dose going into phase III. So that is the one of the primary things you will.
Information you will get midyear, when we kind of do our final download on the phase one trial.
As it relates to how we're going to do the phase two the second issue is what I call. The duration issue I mean currently if you look at any of the amyloid studies.
Both.
Biogen and low like they are both 18 months studies.
To me 18 months in drug development. The due in 18 months studies the minimum two years, probably closer to three years, Matt I'm getting old fast I don't want of have to wait three years to do a phase III study and then another three years to do a phase III study we think.
That if with all of this sophisticated.
Biomarker analytics that we have in place we can shorten the trial in other words, we don't think of it has to be 18 months I don't know, whether we can cut it in half or what yet but that is the second.
Question, we plan to answer.
In the next few months before we really.
Publicize the design of the phase III, so dose duration and the third thing is design, which is just kind of fine tuning the the.
The cognitive endpoints. So we make sure we have the right one because our goal.
Once we once we launch the phase III trial is that it's going to be of trial that hopefully not only enrolled quickly, but it's short enough. So we can.
Maybe we can do a nine month trial and then the registration trial of nine months and basically we get to the market and the same amount of time that it takes for a more traditional amyloid 18 months trial to do their registration trial I E. The Lilly situation. So that's what you can expect in the next few months as I meant.
With Tom Shrader, not only of Youre going to see data on more patients, but youre going to see the three DS dose duration of design and when we talk to you mid year, we are going to be very explicit about those elements and be very explicit about what the phase two trial. It looks like we expect to treat our first pay.
<unk> in the fourth quarter don't want to give you a date or time or a moment, yet, but we're pretty comfortable with that.
With that plan.
Thank you. Thank you for taking me of course.
Our next question comes from Daniel Carlson with <unk> Research. Please proceed with your question.
Hey, guys. Thanks for taking my questions are two.
Two questions first off.
With regards to <unk>, we know that you reduce none of them from Lee inflammation.
Inflammation wondering if you think this will have any impact from the long COVID-19.
Well I have been waiting for that question Dan. Thank you. So we have been very interested since day, one when the early symptoms of <unk>.
<unk>.
Sense of smell and taste were identified we have been looking for a strong signal that there was any neuro inflammatory component quite frankly and I'm. So I'm talking about we've been looking at this for a year.
And as you know some of the price other than shortness of breath of the primary symptoms of <unk>.
Long COVID-19 appear to be no.
<unk> they are <unk>.
<unk> fog they are.
<unk>.
The T. There of depression, and there's plus or minus sleep disorders. Those look like the CNS symptoms, but until literally two or three weeks ago. There was not a convincing publication.
Net neuro inflammation played a role here and the last thing we wanted to do was.
Launch on a quixotic.
Clinical trial.
So we continue to watch this very closely you can imagine we're very interested and I think that there'll be more information coming down the pike on the role of neuro inflammation if.
If the knot.
I don't even need of consensus is if there is a.
Building a bit of data that suggests neuro inflammation plays an important role in lawn Covid you can bet, we're going to have serious conversations about this because 10% at least 10% of <unk>.
Patients with Covid, 19 infections and up with long COVID-19 symptoms and they can be quite.
Quite debilitating so 10% of the millions of patients is the <unk>.
Very big opportunity and if it is neuro inflammation.
We might have the drug that should be tested in the disease. So all I can say Dan is youre right, but stay tuned no decisions have been made yet.
Okay. That's great. Thank you next question.
Can you can you tell us how many patients have passed the 12 week period at this time and and importantly in my mind, how many of them.
I guess the three in the lower dose are not still on the drug but in the higher dose how many of those are still on the drug at this time.
Yes so.
So, yes, the lower dose or not on the drug.
That was more a it took us a while to get the amendment in place for the continuation trial. They wanted to be on the trial, but we didn't have the regulatory elements in place so of the six patients in the high dose group.
Everyone enrolled for the extension trial. So all patients are eligible for nine months additional therapy three of those patients have.
Reached their one year anniversary and have two of those three have applied for special access. So they will continue on drug and Australia. The way they have a system, where you kind of vague.
The physician and the patient and the company can petition the government to allow them to stay on drug. So currently we will have.
Two of the three that are beyond the year that has have been approved for the special access program and the third one is in the process. We just havent had approval yet on that.
So I guess the way to look at it as they are quite.
I mean, the patients and their physicians think of the drug is working right or let me put it this way the patients and their physicians feel that.
They want to stay on the drug and we believe that's a positive sign.
I agree.
One of the say congrats on tapping the ATM I think of those great job in the thanks for the you guys are doing a great job. So keep up the good work. Thank you.
Our next question comes from Brett Conrad with long Longboard capital. Please proceed with your question.
Hello, Yes.
Actually one of my questions got answered by Dan the question, but I have the second one two of them.
The trial and given the kind of current rate of enrollment in that can you give us some general.
Dates in terms of when we expect to get a data readout.
And if that's positive how long it will take the kind of complete the whole thing with the the additional 166 patients.
So as I said, we in the in the presentation.
We expect to reach the.
The DSM V Mark for the first 100 by the end of the second quarter.
And assuming we get the Green light to go forward, we would expect to complete that enrollment.
You know I think.
I think is reasonable.
Unless the unless the disease just disappears with the vaccinations, but you know that ain't going to happen, we're not that efficient and there's going to be enough.
People, who aren't vaccinated out there to keep the the disease in the news so to speak so it is a.
Our.
First goal is to reach the go no go no go no go decision by the day SMB I want to remind everyone that this is not really of data.
Read out the only thing they can do is say stop the trial because.
The things arent working or continue to enroll which would be a sign that debt the things are probably.
Behaving appropriately, but we're not going to get any kind of day to report that says you know 50 patients did this 22 patients with that et cetera. That's just the not the nature of of the the data readout as the trial is currently designed.
Got it got it okay, and I know that the.
That makes sense because of the double blind you only actually even know until it's all over.
You you guys won't even be able to look at those interim data points sounds like no exactly.
The medical you know one of as you know.
We're two hats on both the CEO and the Chief Medical Officer. So on the medical monitor the company medical monitor there are external medical monitors for also so I see all of the reports of.
No problems with the patients, but I can't tell.
I can't tell anything about whether they've gotten the drug or not I can guess, but.
This is not of this is not I don't do that I've been doing it long enough you don't make guesses. So it's the.
The FDA is adamant and we agree that the need to be blinded placebo controlled trials and that's what it is and its frustrating as hell, but it's the right way to get the right answer.
Are you guys seeing any.
Changes in the FDA in terms of the lately.
In terms of getting treatments for Covid.
You see that changing as the diminishes or do you think just.
Just kind of what's your kind of opinion.
The opinion, because I know they also come and go.
The FDA does in terms of there.
The decision.
And emphasis.
So Janet Woodcock, who I respect isn't.
Is a very experienced the new director of the FDA and you can see some changes occurring in some areas I have not had any sense of that and COVID-19, but thats.
The personal one company experience, but you know I mean, the FCA deserves a lot of credit for the way they've handled the pandemic.
And you know Janet Woodcock is I couldnt, we couldnt I couldnt be happier to have her leading the agency she does whats right for patients.
And if you.
If you take the approach that we do that you know, it's all about what happens at the bedside.
I'm confident that the FDA will respond appropriately when we provide them good data.
Great. Thank you.
Our next question comes from Michael Erwin with Universe Securities. Please proceed with your question.
Hi, Michael or when the unit growth.
I have one question.
Oh, okay any of them.
The person. So there's no reason to indicate the depression Ah patients with the crushing are more likely to grow of Alzheimers disease by about one five years and as far as being tackled for both of them.
And the progression of how do you see the affecting exports.
Okay.
Yes. Thank you that's a pretty interesting question actually the way I interpret that data it shows how neuro inflammation cuts across all of these various diseases. So.
The neuro inflammation contributed to both depression in Alzheimer's disease, and there are some people that get both right.
Actually there's also a lot of patients with Alzheimer's disease actually have depression is a symptom of minutes recognized as one of the symptoms and I believe theres even of drug approved for treatment of depression, and Alzheimer's disease. So it's there's no question that theres an intersection the intersection though is.
<unk> two of common pathology, that's neuro inflammation and Thats exactly what Alf.
What extra $50 95 is targeting neuro inflammation and neuro inflammation, if you get rid of neuro inflammation we.
The animal data suggests good things happened in the brain and we're beginning our clinical data at the beginning to sport.
Debt when you get rid of neuro inflammation positive things happen in the CNS.
Alright, thank you.
Okay.
At this time, we've reached the end of the question and answer session I would now like to turn the call back over to RJ for closing comments.
So thank you that concludes today's call. Thank you for joining US we look forward to our next quarterly update.
All I can remind everyone to please.
Get vaccinated and where your math, even after year vaccinated and we'll speak to you again in May.
This concludes the conference.
This concludes today's conference you may disconnect your lines at this time.
Thank you for your participation.