Q1 2022 INmune Bio Inc Earnings Call
[music].
Greetings and welcome to the immune bio first quarter 2022 earnings call.
Okay.
At this time all participants are in a listen only mode. A brief question and answer session will follow the formal presentation.
Anyone should require operator assistance during the conference. Please press star zero on your telephone keypad. As a reminder, this conference is being recorded a transcript will fall within 24 hours of this conference call. At this time, it's my pleasure to introduce Mr. David Moss co founder and CFO of immune buyer, David the floor is yours.
Thank you Paul and good afternoon, everybody and thank you for joining us for the call for <unk> first quarter 2022 financial results with me on the call is Dr. RJ, Tessie, CEO and cofounder of <unk> bio who.
Who will provide a business update on our DN TNF platform.
Dr. CJ Barnum head of neuroscience, who will speak about both of our phase II programs in Alzheimer's disease, and our phase III program in treatment resistant depression.
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 provision of the private Securities Litigation Act reform.
Of 1995. These statements involve risks and uncertainties that could 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 in 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 date. They are made as 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 to start I'd like to state that we were very optimistic about the developments on our two platforms, Inc. Being from NK cells and EXPAREL for CNS indications.
Both platforms have significant potential and we like to say, we like to say that what we are pursuing today is just the tip of the iceberg.
To update you on our progress I'd like to turn the call over to Dr. RJ, Testy cofounder and CEO of immune bile RJ.
Thank you David and thank you everyone for joining the call as usual I will arrange my remarks to highlight the key takeaways for the first quarter and subsequent period and provide updates on our platform programs.
I will start by reviewing our developments and the developments in the ex broke programs.
And I will then hand, it over to Dr. CJ Barnum VP of CNS development to speak about those programs in detail.
And obviously, David will finish with the financial results and upcoming news.
Millstones before we move to Q&A.
We recently announced the dosing of the first patient in the phase two extra trial for the treatment of neuro inflammation is a cause of cognitive decline in Alzheimer's disease and immune by believes that restoration of synaptic connections and prevention of nerve cell death with extra therapy will have a pro cognitive.
Effect on patients with Adi.
Adi that's capital a capital D. Small oi is the term we use to define the 80 patients with neuro inflammation that are the target of our clinical programs in Alzheimer's disease.
The design of the Phase III Adi trials are based on what we learned from the successful phase one trial the use of Biomarkers help select dose duration endpoints of the trials to derisk the programs.
These biomarkers irrelevant beyond Adi and provides new opportunities for the staging and treatment of CNS diseases.
The opportunities to you extra extra beyond Adi are real.
Alzheimer's disease is the first of the neuro degenerative diseases will be taught.
Treating with <unk>.
We have announced the program phase II program in treatment resistant depression or <unk>.
In depressed patients with neuro inflammation, something we call <unk>.
And our performing IND, enabling preclinical studies in ALS each of these programs.
With extra mural non dilutive funding from the Alzheimer's Association, the NIH and the L. S Foundation, respectively neurons.
<unk> inflammation is the common denominator of the CNS indications more than 70 publications covering more than a dozen diseases. It gives you a hint of the opportunities before us.
These publications can be found on our website.
We will be enrolling additional patients in the coming months in the phase II mild Adi trial.
We will be initiating our phase II Mci trials soon.
But first during the first quarter, we presented additional data from the successful phase one trial at the 80, PD 2022 conference in Barcelona, or imaging Parker partner in Mecca demonstrated that measures of white matter pathology are different and Mci versus Alzheimer's disease.
These patients.
And may provide a means of predicting progression from Mci to Alzheimer's disease. These data have implications for our clinical development programs and drove our decision to separate trials in Mci and mild Adi.
In the future the ability to identify patients at risk of a conversion from Mci to E D.
<unk> Z may prove to be a key step in preventing the development.
Of dementia related to outsiders disease.
Well I started in Mci trial now the answer is quite simple there are two elements necessary for drug approval clinically relevant efficacy data and an ample safety database by adding the Mci trial, not only do we get insight into a clinically and commercially relevant market beyond.
<unk>.
But we also expand the safety database.
Both of these trials will help us achieve our goal of moving extra closer towards registration trials.
Jay Bar and I'm, the VP of CNS development at immune bile and the architect of our 80 trials will provide more detailed information on.
Our Alzheimer's disease clinical program C J.
Thank you RJ.
<unk> bio will be conducting two phase III trials in patients with Adi.
One in <unk> that is currently enrolling in a second and Mci that will begin enrolling later this summer.
The three most common questions, we get asked or why are we doing separate trials in Mci and mild AE why are our trials small and shorts and why do we use non traditional primary cognitive endpoints.
First I want to reiterate why we are bullish on the use of EXPAREL to treat Adi simply speaking neuro inflammation causes dementia. The evidence for this is overwhelmingly supported by preclinical genetic and epidemiological studies.
Soluble TNF target of X Pro is the master regulator of neuro inflammation and modulates the activity of nearly every inflammatory target in development for <unk> in short we believe TNF is the most important inflammatory factors driving even.
More importantly, we have a drug that neutralizes the species of TNF that drives dementia soluble TNF and preserves the part of TNF that is necessary for CNS repair transmembrane TNF, we believe that the drug may be pro cognitive precisely because it preserves trans membrane.
Mediated neuronal repair.
So far this hypothesis has been supported by our non clinical and early clinical studies.
But back to the questions I mentioned earlier.
We are doing separate trials for Mci and <unk>, because the biomarkers are different for each disease by separating them into individual studies, we will get a clearer picture of how our biomarkers are changing.
Second patients with Adi progressed rapidly and reliably.
I want to emphasize this because it is not widely known that patients with increased inflammation.
<unk> faster and with more consistent progression between patients.
This clinical reality allows for trial design advantages the most prominent being adequately powered smaller and shorter trials.
Finally, we have chosen scales that measure cognitive changes that occurred during mild EDI and Mci our primary endpoints E. Mac was empirically derived to measure targeted changes in these early 80 patients, whereas Adas cog was developed to capture.
<unk> changes that occur in moderate and severe <unk> patients.
The cognitive changes that occur in early <unk>.
Our different from those that change in moderate and severe disease, and therefore require a different scale. The E. Mac is that scale.
The NCI study is a blinded randomized placebo control study of <unk> in patients with Mci due to this.
This proof of biology study will enroll 60 patients in Australia, and North America patients will be randomized two to one drug to placebo, where they will receive X pro for three months.
The primary goal of this study is to determine the effective X pro on cognition and Biomarkers that will inform the design of a registration trial.
Why is this important NCI studies are plagued by a slow rate of cognitive decline and low rate of conversion to <unk> Dx.
<unk> extensive biomarker package, we are using in the Mci trial will help us derisk the registration trial and dictate if mci and mild <unk> can be studied together are must be studied separately.
To reach this goal, we used frequent and diverse clinical and biological measurements of cognition inflammation neuro degeneration and function.
This strategy decreases risks and increases the probability of success spin.
Specific information about this study can be found in clinical trials Gov.
Our phase two proof of concept study in mild patients will enroll 201 patients with Adi.
This six month randomized blinded placebo controlled study is powered to show a significant effect on the primary and key secondary endpoints of cognition as described above for the NCI trial, we are using endpoints that measure the cognitive and clinical or changes that occur in patients with mild <unk>.
<unk> disease, we are confident we have designed the study that will succeed and provide a clear path for a registration study as <unk>.
Jay mentioned above we have started treating patients and are on pace to meet our timelines.
A feature of both the mild EDI and Mci trial is that once patients complete the six and three month trials respectively.
All patients will be offered Expo for opportune additional 12 months during that time, we will obtain additional data on safety and efficacy that will add to our clinical and safety database.
We believe the short timeline of the trials and the fact, all patients will be able to grow on X pro will be an attractive recruiting feature for patients.
Now I will turn to treatment resistant depression.
There are approximately 7 million patients per year in the U S with treatment resistant depression, approximately one third of those patients will have biomarkers of neuro inflammation that we believe is it cause of their treatment resistance.
Proof of concept studies with nonselective TNF inhibitors have demonstrated a therapeutic benefit for patients with treatment resistant depression and biomarkers of inflammation.
We have announced a phase II trial of <unk> in treatment resistant patients supported in part by a $2 9 million grant from the National Institute of Health.
This study is a six week blinded placebo controlled study of <unk> in 90 patients with treatment resistant depression and biomarkers of inflammation.
<unk> with our <unk> development strategy, we will select patients with biomarkers of inflammation.
The primary endpoint will assess the impact of EXPAREL on the functional activity of the reward pathway in the brain.
This functional MRI metric is a well documented change associated with inflammation and key depressive symptoms, including antidote and motivation, which alongside with traditional depression scales will be assessed as key secondary endpoints.
As with Adi the enrichment strategy and target engagement for TRT patience with neuro inflammation aligns the path ology of the disease with a mechanism of X pro.
More information about this study will be available as we get closer to the start date.
Now, let me pass the call back to RJ to discuss our second platform.
RJ. Thank you C J.
<unk> is our proprietary natural killer cell priming platform that we classify as a suite of Cod why do we call income in a suite of kind of all other NK companies that use NK cells as their primary therapy requires cytokines to support prime and expand their NK product into an effective therapy.
Cytokines are a problem they have Texas toxicities, when given directly to the patient either alone or as part of a multi cytokine cocktail.
Toxicities can complicate the management of a sick patient population cytokines are expensive and cumbersome when added to a complex manufacturing process.
We can solve these problems in an elegant manner by converting the patient's own NK cells, while they are in their body in their own circulation into the cancer, killing memory like phenotype without the need for cytokines genetic engineering or ex vivo culturing or processing and <unk>.
In a safe and simple.
We have seen the effectiveness of increments therapy in two of three patients with Mds AML.
And we expect this approach will differentiate inkerman therapy from other NK cell strategies.
Like you, we are frustrated and our inability to recruit patients into the <unk> trial to solve this problem, we have expanded our clinical trial.
In the Mds program to include AML patients. In addition to the Mds patients even in the era of Covid.
Ml patients must come to the hospital for their treatment.
This eliminates one barrier to enrollment.
We are working to open a second site in the EU and we believe these two changes will allow us to obtain additional incremental patient data this year.
Why is it that most NK targeted therapies focus on hematologic malignancies, It makes little commercial sense since more than 90% of cancers or solid tumors.
That focus is based on biology, NK directed therapies do not work well in solid tumors.
Mark with Dell has discovered why NK cell therapies don't work in solid tumors and it's actually quite simple.
Tumor micro environment, where NK cells must perform their magic is very inhospitable to NK cell function.
The TMA is hypoxic and immunosuppressive.
What is what is a hypoxic tumor microenvironment hypoxia is abnormally low oxygen levels that prevents a cell from working normally think about when you go skiing in Colorado. When you first arrived you can't walk up a flight of stairs without getting short of breath, the oxygen level at 9000 feet.
30% lower than at sea level, you feel it.
Like you when the NK cell is hypoxic it cannot survive and thrive and it certainly cannot kill cancer cells.
<unk> appears to solve this problem by up regulating mitochondrial survival proteins and nutrient receptors compared to cytokine primed NK cells. This is probably why England prime to NK cells thrive survive thrive and kill cancer cells and the hypoxic TMA.
NK cells that are produced in normal oxygen levels, just don't work to our knowledge every NK company produces their NK cells and norm OXEA.
The immunosuppressive environment of TMA is the second problem that has overcome by increments compared to cytokines.
Cytokine prime to NK cells primed NK cells kill cancer, when surrounded by immunosuppressive tumor activated macrophage macrophages Mds cells and T regulatory cells that are all trying to protect the cancer.
Priming within <unk>.
Produces a memory like NK cells that kill and kill and kill again.
And the patients that responded to <unk> memory like and G. K <unk> positive NK cells that's the.
Memory like NK cell that has cancer, killing were present in the blood and bone marrow for at least 100 days after the last dose I think to.
To our knowledge this.
Prolong therapeutic persistence is unmatched by cytokines.
Avidity is a measure of how effective the NK cell killing of cancer cell.
More avidity is good for controlling cancer.
<unk> causes the higher much higher avidity.
And then any side of single cytokines and assays of.
Cancer, killing.
Professor Waddell presented this in more at the innate Killer conference last month in San Diego, where he chaired a session on the use of NK cells in the treatment of solid tumors.
<unk> is ideally suited for treating solid tumors.
Does it advantages we are pivoting towards solid tumors, a market that is many times larger than the liquid tumor market.
We are not abandoning the Mds AML program. It is important source of information and insight for clinical teams the company and the regulatory authorities.
We will take what we're learning from Mds AML to move forward in solid tumors.
You already know about ovarian renal cell a nasopharyngeal cancers both.
Preclinical and preclinical stages, but this is just the beginning solid tumors are the future of <unk>.
At this point I'd like to turn it over to David Moss, our CFO to review certain financial items.
Thank you RJ I'll provide a brief overview of our financial results and upcoming milestones before we head to Q&A.
Net loss attributable to common stockholders for the quarter ended March 31, 2022 was approximately $6 9 million compared with approximately $4 6 billion for the comparable period in 2021.
Revenues totaled approximately <unk> 2 million for the quarter ended March 31, 2022 compared to zero.
For the comparable period in 2021.
Research and development expense totaled approximately $4 3 million for the quarter ended March 31, 2022, compared with approximately $2 5 million for the comparable period in 2001.
General and administrative expenses was approximately $2 3 million for the quarter ended March 31, 2021, compared to $2 1 million for the comparable period in 2001 2021.
Other expenses was approximately <unk> 4 million for the quarter ended March 31, 2022, compared with zero for the comparable period in 'twenty one.
At March 31, 2022, the company had cash and cash equivalents or daily just cash of approximately $66 7 million I'd like to point out that during the quarter as previously reported in an 8-K filed with the SEC. We sold 82900 shares to officers and directors for approximately <unk> <unk>.
100000 in cash that includes RJ, Mark Lidell myself and one director.
Based on the current on our current operating plan. We believe our cash is sufficient to fund our operations into late 2023.
As of May five 2022, the company had approximately $17 9 million shares of common stock outstanding.
Now I would like to move on enlist our upcoming milestones and catalysts before Q&A.
As previously highlighted by both CJ and RJ, we dosed, our first patient in our phase II <unk> $15 95 trial for treatment of neuro inflammation as a cause of Alzheimers disease, we expect.
To continue enrolling patients over the coming months in order to reach our enrollment target of 201 patients.
Topline results for the six month program is expected in late 2023.
In the first half of 2022, we plan to initiate a three month 60 patient phase II program for mild cognitive impairment.
Barry.
The unexpected delays, we anticipate having top line results sometime first half to mid 2023.
In the coming months, we plan to initiate a phase two trial of <unk> in patients with treatment resistant depression.
This is partially funded by a $2 9 million Grant NIH grant.
We expect further open label high risk <unk>.
Ml data in EP and patient as the program continues to enroll.
Finally, we plan to launch a second <unk> study in ovarian cancer or another solid tumor in 'twenty. This year in 2022.
So in summary, we're pleased with our progress for the quarter as we continue to advance our pipeline towards potentially evaluate creating milestones.
At this point I'd like to thank you for your time and attention and I'd like to turn it back to Paul to pull for questions Paul.
Thank you we will now be conducting a question and answer session.
I would like to ask a question. Please press star one on your telephone keypad, a confirmation tone will indicate that your line is in the question queue you May press.
I'll start too if you'd like to remove your question from the queue for participants using speaker equipment and may be necessary.
Pick up your handset before pressing the star keys, one moment, please while we poll for questions.
Yeah.
Thank you. Our first question is from a young man Tommy with B Riley Securities. Please proceed with your question.
Hi, This is William wood on for Mike.
Today I really appreciate the update that you provided.
Congratulations on all the progress.
Yes, as you've been making.
I've got a couple of questions the first.
Focused on your Mci and <unk> trials.
So your the NCI earlier.
Earlier population I was going for three months.
Mild.
More severe population in the trial is running for six months.
I guess could you just yeah, just curious thinking.
Thinking about the limits of the Mac.
And.
How you see these two trials with the Readouts in the difference in populations and the difference in timeline, maybe in my eyes, the less severe trial should be potentially longer and are a bigger.
Just curious about your thoughts on that.
Yes, thanks, So Jim I'm going to let Jay answer that.
So I mean.
It's a really long answer it's a good question, but theres a lot of elements to it.
I think referring back to what we said in the.
The call we view these in some ways, it's two different diseases and if NCI is viewed as a different disease, we need to make sure we understand that our biomarkers work that we're looking in the right spot before we put a lot of time and resources into it. The other factor that is involved in the length of these studies has.
To do with what you expect.
So if your expectation for example is just slow decline of the disease by 50%.
Dictates, how long the trials need to be.
If you expect the drug not to <unk>.
Patients will start progressing that's obviously a different timeframe and we actually have different expansions expectations between mci and mild patients, but really the truth is the reason we do a three month study is because we need to understand if our biomarkers are working and that Mci population.
Before we move into a more proof of concept and we need to understand the conversion rate as well and how our biomarkers reflect that yes, let me jump in here.
I am also I mean, we just spend a couple of days with the team and that included Judy Yeager, who we've mentioned before.
<unk>.
Our cognitive Guru and really one of the architects of being back and one of the important points. She made reinforces what C. J just said it depends on your expectations if you're expecting.
To differentiate the two between two declining population Juno need more time, you need more patients as we've said many times, we are expecting our patients to be euphemistically say flatlined or stable. So we arent expecting our patients to get worse in a vacuum the mci.
Patients there is even a chance that we will have a better outcome to that that really changes the.
Shall we say the opportunity for <unk>.
Demonstrating.
Meaningful way the effects of the drug so once again it goes back to the lack of sensitivity of the traditional Adas Cogs, which is just <unk>.
Completely inappropriate for Mci for sure mild a D for sure.
And using a more sensitive tool suddenly allows us to be more confident of our development one more comment by C. J, yes. So let me address the cognition piece because I think that's important.
Yeah.
We've been saying this all along that you sort of you have to measure what's.
To be able to measure what's changing and we believe the Adas cog just doesn't do that.
So this is why the <unk> was empirically derived was really determined to do that now the field understands this is a problem knows the ddos cognizant very good.
Convention is a problem in this business.
You have to remember that our secondary endpoints used CVR the CBR is.
A an endpoint that can that we know can be used in registration studies and we powered the studies.
Based on the CVR as well so even though we believe the <unk> will be superior and we think the <unk> will be developing <unk> in a way that will potentially be able to use it as a primary endpoint in our registration trial, we have the CD R&R back pocket to make sure that we're covering all the bases.
You had a second question.
Yes.
A quick one and then two quick ones.
Don.
It looks like at least in general and your timelines have been slightly pushed back at least from your fourth quarter, just trying to get a feeling on how we should interpret this.
No.
We said we'd have the Mci the first first half of the year.
<unk>.
The mild Adi in the second half of the year, that's exactly what we plan.
Okay.
I'll take that and then I guess lastly, just on your income in trial.
Obviously, it's not an inquiry incorporating the AML patients.
Just trying to get.
Feeling on how we should be viewing that trial going forward, obviously, you said you'd be still.
Still treating the MLS but are you going to be trying to enroll both <unk> and.
The extra color would be appreciated. So so yeah fair question. So we've expanded the inclusion criteria now to include.
A number of AML categories patients with incomplete response to chemotherapy with circulating blast that aren't candidates for a bone marrow transplant patient who have failed a bone marrow transplant for AML and Theres, one other criteria to that and blocking up. So these are all being lumped into the same trial now so theres not two trials.
It's one trial with high risk Mds, which is a pre AML and bad actors on the AML side and as you know this is a biomarker driven trial that we've actually had some pretty good responses I mean remember the both of these patients are more than six months out after their last dose of <unk>.
Anthony and with complete control of their disease on no. Other therapy. So now we have a cure them because they still have disease, but these patients are living normal lives. So.
I think the way to look at it is really as I described it in the last paragraph we like what's happening in Mds AML. We are frustrated as heck that we can enroll the trial and I can tell you that anybody who's enrolling AML Mds trials is having trouble enrolling patients because it's way too many companies.
<unk> way too few patients.
The reason I went in such detail on the ability of ink immune to positively affect NK cell function and the TMA is because we believe solid tumors is a huge opportunity for inc.
That will dramatically differentiate us from other companies no other company to my knowledge has.
Presented every evidence of why they are not approaching solid tumors. We now know why we should attack solid tumors and we think that's the future for the product now.
Okay.
The proof is in the pudding and that means we need to open the ovarian trial, we need to open other trials when we have some interesting plans afoot.
What you'll hear about we will finish the Mds AML trial, but I do believe in.
Saying it publicly here that the future opportunity of bank.
Solid tumors and there is only nine times the number of solid tumor patients than there are hematologic malignancy patients.
Yes.
Thanks, Glenn I appreciate the extra color there congratulations again I'll jump back in the queue.
Yeah.
Thank you. Our next question comes from Matthew Cross with Alliance Partners. Please proceed with your question.
Hey, guys. Good afternoon, and thanks for taking a couple of questions from me.
I'll jump on to the kind of line of discussion here regarding.
NK cells are intermune.
Within solid tumors, which I think.
Accurately as probably the direction to be going.
The question that I had was I guess, how do you envision actually moving into the solid tumor space.
I guess exactly as RJ.
You pointed out that there isn't really much in the way of data or certainly nothing all two promising yet from any of the other allogeneic NK cell therapies, we were delivering actual.
Cells.
Or NK cells in this case into patients in the solid tumor setting so I guess with another experimental agent like <unk>.
Need to wait for the <unk>.
Cargoes or whichever allogeneic NK cell developer.
The world to kind of paved the way getting approval in solid tumors.
Et cetera et cetera in order to prove that you can use <unk> to really in these aggressive solid tumor types enhanced avidity and others sell functioning metrics or.
The way you've described it do you need to kind of look at improving residual disease and those solid tumors.
Patients normal and maybe in a cancer patient.
More suppressed NK cells can be rejuvenated to some extent.
To sufficiently fight disease, I guess, you need to wait for the rest of the field to catch up.
Or can you really go into even in these very aggressive solid tumors right away right now.
Just maybe this isn't the way to put it.
So all I can say is hell no.
There is not a reason that I can think of why we would wait for everybody to catch up they are clueless quite frankly about how to attack solid tumors, because they really don't understand what's going on in the tumor microenvironment and if theyre set well they may understand but they've never to our knowledge.
Studied.
The function of their cells in the environment that theyre going to be meeting and the TMA, our top secret program or secret our top secret shall we say sauce here is mark with Dow Mark with Dell has been studying NK cells may.
Maybe not 30 years, but certainly 25 and he has really studied this and basically now as I presented understands it well I think you bring up a point that's important though youre talking about these patients with.
Aggressive bulky disease.
What will differentiate us I think in our program. So we're going to be careful about picking the cancers.
Mark has criteria based on NK infiltrates, a biopsy some kids et cetera about cancers. He wants to talk tack I'll, let him comment when he is able to join us on the call more specifically.
But so there is only certain cancers and we are sensitive to the fact that we don't believe in commune is a magic bullet for people with bulky diseases. We will ideally go after patients with a low burden of disease.
That we can that won't be that way.
Don't necessarily concurrently with with chemotherapy may be with other immunotherapies, but the fact is we will pick and choose our battles in a way that allows us to.
Tak certain.
<unk> of <unk>.
Patients within the cancers that I've talked about so stay tuned we have something to learn but the most important thing that I presented today, I think and what Mark really talked about when he was at the innate killer conference was that.
We now know why everybody has failed in NK cells and <unk> com.
Solid tumors, because they keep making NK cells that are supposed to be working in 21% oxygen with no immunosuppressive environment throw them into the patient and they get blindsided by hypoxia and immuno suppression.
And commune NK cells work in that environment and to our knowledge, others don't and if I'm wrong I'll be the first to admit it.
But so far nobody has any data other than us and that gives us confidence.
Understood Super helpful. Thanks RJ.
And I think on switching to the Mci side quickly for one question.
I think what im, particularly wanted to focus on was the upcoming study in T. R. D. As I think you guys covered quite a bit around ADL Mci.
But contrasting TRT with ADL Mci.
And those latter two youre looking at patients that have neuro inflammation also vacation CRD, but.
In both of those cases, where <unk> Mci youre looking at patients allows amyloid in your question in the equation.
For Mci I think they need to actually be amyloid positive to enroll.
So since amyloid I guess, it's a pretty well documented trigger of microbial activation and that inflammation that expert should normalize in patients I guess in.
In the case of something like CRD or Parkinson's or other.
So when they go on that iceberg a potential infill.
Neuro inflammatory diseases.
Could you kind of comment on how you and richest study in those other indications where glial cell activity isn't really a central to kind of mechanistic rationale and you can't filter patients by amyloid.
C J.
Yes, so the simple answer to that question is as we do I view amyloid differently I don't think amyloid as necessary if you have inflammation.
That's the patient we're looking for and that biomarker is going to we believe we will be able to identify and identify the biomarker that will tell us which patients have inflammation in the brain and those are the patients we're going to select so in the case of treatment resistant depression, we already know.
Patients with high CRP blood levels of CRP respond to anti TNF therapy.
That data has been published previously.
If you look at it the TNF inhibitors and other diseases that are currently on the market CRP is used as a predictor of treatment response. So I think we don't need a next level for these diseases.
Think we need to make sure that CRP is the best.
Biomarker, there may be better Biomarkers will unravel that overtime, but but I think it's I think we just need to focus on the patients that have inflammation and if I could make one more comment here one of the key elements for C J and immune buyout to win this large funding.
Tranche from the.
NIMH, which is National Institute of mental health was the fact that.
You've mentioned earlier and nichol, the patient with the elevator information because of it faster and more consistent <unk> disease progression. So I'll just wondering Ed what clinical disease stage is that like a fast right up disease progression like step global <unk>.
To those.
With the <unk>.
Non elevator inflammation and I have a follow up for a second question actually.
C J.
It's a good question. The answer is is it doesn't really matter.
Where they are in the stage of disease, what matters is whether or not they've got the biomarkers of information if they have the biomarker of information and you look over the course of the next.
Six months 12 months or however, you want to look at it their disease progresses faster.
And the most important part is that the variance and disease progression between patients as low and that gives you enormous power advantages to do smaller shorter trials.
Okay very helpful. Okay, and then the second part second question is so regarding the depression. So you mentioned earlier that refund inflammation influences the different Tribune responds, but are there any data to suggest that the combination therapy between anti depressants and anti inflammatory may have like a synergistic effects.
And how establishes a roll of inflammation in other indications such as schizophrenia or bipolar disorder.
So great question I think the jury is still out on that we don't have a lot of we don't.
The point, where the jury is still out on whether a combination with for example, X pro and an SSRI will be any more advantageous I think most of the studies that have really looked at inflamed depressed patients have looked at cohorts with.
Trauma related onset, which is a uniquely different disease.
That that.
Where where are the combination of the two may not be as effective but we don't know the answer to that [noise].
And what was the second card a friend so so schizophrenia bipolar.
These are patients that have documented inflammation in fact schizophrenic patients have some of the most the highest levels of information I've ever seen in the brain.
Those are really unique circumstances part of the the the issue. There is these are developmental diseases, where the brain gets rewired a certain way.
And it is not clear whether you can make a difference once the disease has onset. So it's not a program that I will be tackling anytime soon.
Great very helpful. Thank you.
Thank you. Our next question is from Daniel Carlson with T. W Research group.
[noise] hi, guys. Thanks for taking my questions.
Yeah.
Regarding <unk> you know a lot of people have suggests that you're not getting much market for this and one of the better days you've had recently was when encarta came out with the results. So I'm just wondering if you could talk about.
What in their results bodes well for ink knees and Beg me program and and also what is the difference between you guys in there for that.
So so thanks, Dan I'm going to let the Ah David start with that answer and then maybe I'll jump them. So you know a number of different things you know I think that I'll point out that it's very early at it in case L land. They only talked about six patients. Obviously, we only have a few as well, but we're intent unenroll anymore.
A big part of it is the phenotype of the Yankees, so that they're using which is S. N K G T D plus positive cell.
You know, obviously I think I was a little bit surprised at the at the market response.
I think another part of it is that.
They're seeing.
They have a car that they're using to to help get the activities he need with their incase L. And obviously, we get the same type of activity without the use of a car or the complications related to.
Side effects with the which they use and then I think the jury's out about.
The persistence.
Ah therapy, and the number of doses that that are needed. Obviously, you know we're monitoring our patients over a long period of time with persistence, we need to get we need to show more of that and more patients.
And you know hopefully if we're able to do that the market gives us credit similar to what they've done with other encased all companies, but I would say to date.
We we feel is a company that we do not get the credit.
Of of our Incase they'll program, but we believe that will come with additional data, which is what we're very focused on delivery. Yeah. Let me jump in here and make a very important point. The reason car T cells work and the only reason they work is when they actually in graft that is those.
Car T cells can be found many many months.
Probably years after the patient has been treated in the patients that remain.
Shall we say free of disease patients as soon as that Engraftment as lost those patients tend to relapse <unk>.
In case else don't of graft and that's not the case. So you know putting a car on and in case L may do something for it it's not going to alter your therapeutic persistent switch as I've already told you is a key element to how well you can control the tumor one so one made.
<unk> advantage is right now we have a best in class therapeutic persistent maybe it isn't but I haven't seen any data that suggests anybody's even close to us that's number one number two.
The bank. This is you know remember, we're not giving NK cells, we don't have any we.
We don't have to keep cytokines for the patient or cytokines for the manufacturing by the way. The reason many in case cell companies give cytokines is to promote proliferation promote avidity and promote persistence and what they do is promote toxicity and they don't get much of the other three elements. The finally.
And can be as easy to make I mean, we got buckets of the stuff and so it's logistically simple it's cost effective it's safe and well tolerated, we get the right kind of N K salaries memory like NK killers, they have last a long time and the pay.
<unk>, that's a more complicated discussion and back to what I talked about earlier the cell we make will work in solid tumors, because it can tolerate and thrive in that hypoxic immunosuppressive tumor microenvironment.
I got it just switching gears, maybe it's this procedure but.
Talking Alzheimers recently with Big Pictures, obviously, what's going on with Biogen. So I'm just wondering seems like it should be positive for you guys in terms of your recruitment, but if you can just sort of talk about what's going on with them and how that's going to impact you.
Let me start on the business question, because I you know, obviously I get up every morning, and I anxiously look at my news for you and see what's new with the the Biogen So saga right and obviously now they've they've.
The C E O step down and they're really stopping their investment and add it at academy, but people forget that they have an antibody that's coming behind called <unk>, which is once again with a sigh, which looks to be more like to function more like the liliana body than not.
So it's not that Biogen is abandoning anti amyloid strategy. It's just they are you know.
The amyloid the Adam Adam how almost just a severely wounded duck now my interpretation that home data is it and great, but it works and I can tell you people forget that it all three drugs, whether you're looking at Biogen drugs, whether you can <unk>.
Drug of the <unk> the target amulet have about the same efficacy, which quite honestly. We think is subpar and I'll also tell you that there is to date to my knowledge no anti tell therapy. That's had any evidence of efficacy. So I think we know where the old fashioned approaches are.
Where they are going to sit where the anti Tao and the anti amyloid strategies are going to be and it's time to be and I think the communities turning to other approaches.
We are getting.
More mentions I guess, you might say nor inflammation is viewed as important.
We have great preclinical data, we have great phase one data, it's now up to us to produce great phase two data. So you will all understand that when you become 75, you Wanna be an extra.
That's it for me again, thank you very much appreciate that.
So can you.
There are no further questions at this time I'd like to turn the floor back over to RJ for any closing comments.
So thank you all for joining I think.
I think we presented a little bit of new information here with ink and and our increased interest in solid tumors. I think you can hear the confidence we have in the X Pro X Pro program for Alzheimer's disease, and we understand that it's up to us management and the company to drive.
Clinical trial enrollments. So we can give you the answers and.
And have you get us enthusiastic about these programs as we are with that we will sign off.
This concludes today's conference you may disconnect your lines at this time. Thank you for your participation.
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