Greetings and welcome to INmune Bio’s First Quarter 2020 Earnings Call. At this time all lines have been placed on a listen only mode and the floor will open for questions and comments following the presentation. [Operator Instructions] As a reminder, this conference is being recorded. A transcript will follow within 24 hours of this conference call.

At this time, it is my pleasure to introduce Mr. David Moss, Co-Founder and CFO of INmune Bio. David, the floor is yours..

Thank you, [Latania] and good afternoon everybody. We thank you for joining us for the call for INmune Bio’s first quarter 2020 financial results call. With me on the call is RJ Tesi, CEO and also Co-Founder of INmune 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 provision of the private securities litigation Reform Act of 1995.

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 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're made as the facts and circumstances underlying these forward-looking statements may change.

Except as required by law INmune Bio disclaims any obligations to update these forward-looking statements to reflect future information events or circumstances. Now, I'd like to turn the call over to RJ Tesi, CEO of INmune Bio.

RJ?.

Thank you, David and thank everyone for joining the call on these difficult times – difficult and interesting I think is the best way to describe them. I will arrange my remarks to highlight key takeaways for the first quarter, the year-to-date and provide updates from our two platforms.

Then I will turn it back to David Moss to discuss our financial results, upcoming milestones before we open the lines for Q&A. We'll start with the DN-TNF Platform. We have four therapeutic programs and development. These include INB03 for cancer, LIVNate for NASH.

We have a new program that we're calling Quellor for treatment of cytokine storm related to COVID-19, and XPro1595 for Alzheimer's disease. I'll remind you that these are all the same drug from the single platform. I'll start with our newest program, with Quellor, targeting cytokine storm to treat the complications of COVID-19.

We initiated this program after completing a strategic gas assessment, and we are planning clinical trials with the DN-TNF Platform for the treatment of the complications of this disease. Our decision is based on the four TNF related attributes of COVID-19 and the pathophysiology of the disease. The first is cytokine storm.

This is – shall we say a top line problem with COVID-19 and blunting the effects of the cytokine storm makes sense. Soluble TNF is a major part of the cytokine storm, and neutralizing soluble TNF is what DN-TNF Platform does. But the soluble TNF plays two other very important roles that are not as obvious to many.

The first is, that for tissue destruction to occur, immune cells must move from inside the blood vessel to outside the blood vessel, and into the tissue where they cause the damage, soluble TNF when it activates endothelial cells, cause them to upregulate ICAM-1 and VCAM-1.

These proteins are sort of like traffic cops that signal to activated immune cells that are living by in the bloodstream and signal them to stop and exit the blood vessel that's called trafficking into the tissue, where they cause damage.

A more obscure role of soluble TNF is that it contributes to the coagulopathy, which is the cause of many of the complications related to this [indiscernible] disease.

When soluble TNF activates endothelial cells and macrophages they upregulate tissue factor; tissue factor actually starts the coagulation cascade that results in much of the pathology associated with pulmonary, renal and vascular disease and probably neurologic disease, in patients this coagulopathy is [indiscernible] by elevated D-dimer, a biomarker of severe disease and present in almost every – elevated in almost every patient who’s admitted to the hospital.

Working with clinicians and the regulatory authorities, we are moving rapidly to start a clinical trial that will attempt to prevent the catastrophic complications of COVID-19, including the need for mechanical ventilation. We hope to be enrolling patients by July ideally in a program supported by non-dilutive funding.

XPro is being used – XPro1595 is being used to treat Alzheimer's disease, an app to metaphor for this program as steady as she goes. We're confident in our goal to have data for review in October, if not sooner. And we are beginning to plan for the Phase 2 trial, but we admit the pandemic has forced us to be creative.

Future programs must require fewer trips to the clinic without sacrificing the ability to collect critical data or the quality of that data. We have some ideas; we're working to implement them, and we'll tell you more about these in the future.

INB03, our cancer program is being targeted to treat women with metastatic HER2+ breast cancer, especially those with CNS mets. Just a couple of weeks ago, we announced the publication of an invited review and frontiers of oncology, entitled tumor necrosis factor, an opportunity to tackle breast cancer by Roxana Schillaci.

She is the, you know, lead, shall we say thought leader that has been working with us on the role of TNF in cancers, especially breast cancer. And this publication is part of an evolving body of work by Dr. Schillaci and are team on the role of soluble TNF and resistance to immunotherapies including trastuzumab and tyrosine kinase inhibitors.

Just three days ago, Sophi Bruni, a doctoral student in Dr. Roxana Schillaci Lab presented work at the New York Academy of Science frontiers in immunotherapy 2020 meeting. That work demonstrated that a combination of Lapatinib, a PKI inhibitor, and INB03 overcomes resistance to trastuzumab and HER2+ breast cancer models.

This work informs the design of our planned Phase 2 trial in women with brain mets from HER2+ breast cancer. Lapatinib is a dual EGFR HER2 inhibitor. It's part of the [PKI class]. It's a good drug and a difficult disease that suffers from early resistance. We believe we have identified this resistance mechanism.

And we are targeting women with HER2+ brain mets because both drugs cross the blood brain barrier. All of these or most of these women will also be expressing MUC4, which makes them resistant to trastuzumab based therapies.

Finally, the combination increases – decreases myeloid derived suppressor cells and the key immunosuppressive cells in the tumor microenvironment and makes cold tumors hot in animal models, and we hope this sets up this combination to be part of triple therapy that will include immune checkpoint inhibitors.

I would just as an aside, tomorrow, AACR will be releasing their abstracts. This work is also being presented at the AACR. Originally, that was supposed to be the first release of the data, but as with many programs COVID-19 has changed the calendar.

Moving to LIVNate for NASH, giving patients new livers was a big part of my previous life as a transplant surgeon, but there's a surgical saying that says the sign of a good surgeon is the one who can avoid an operation. And that is the goal of this therapy to avoid the need for liver transplants.

We have identified a novel mechanism pathologic mechanism to treat NASH. We believe that LIVNate seals the intestinal leak that is critical in driving inflammation in the liver. The leaky gut results in very high inflammatory cytokine load in the portal vein, two logs greater than what you see in the blood.

The portal vein feeds blood directly from the intestinal tract into the liver, and this highly inflamed [liqueur] has predictable effects on the liver with inflammation, decreased hepatocyte survival, which ends up with fibrosis and changes in the liver histology.

The protocol is written, sites are identified, but we are delaying the initiation of this trial for now. Starting new trials in the COVID-19 era is challenging. Starting trials in a disease that is life threatening is a bigger challenge, and as we ramp up the COVID-19 effort, we are husbanding our drug supply with our existing programs.

We have drug available to complete the Alzheimer's program to complete the plan COVID-19 program, but to support our expanding clinical programs, we have signed an agreement with KBI Biopharma to produce additional drugs. This concludes my comments on the DN-TNF Platform and I’ll move to the NK Priming Platform.

The NK Priming Platform we call INKmune and we have two therapeutic programs in the queue. INKmune will be studied in solid tumor and hematologic malignancies, ovarian cancer and high-risk MDS respectively. The latter is a form of a pre-leukemia.

In April, we announced that the USPTO had provided formal notice of the allowance of a patent application entitled in vivo priming of natural killer cells. This is the first of several that are coming for this platform.

The patent relates to and I quote, “the method of treating cancer by administering a proprietary inactivated cellular material preparation and contacting a patient's own natural killer cells within the body to induce an in vivo response, namely the priming of NK cells for enhancing the innate immune response, and the NK cell ability to recognize and kill cancer cells in the patient.

I'll remind you, we do not give new NK cells. We believe and we have excellent data to support it, that the patient – the cancer patients NK cells are fine. They have all the tools they need to kill cancer cells, but they need targeting assistance. They need to be turned on and that's what INKmune does.

The newly allowed patent is expected to issue in approximately 60 days and will expire in 2036. This is just as I said one of the many of the company's IP or patents that were expanding our portfolio and we believe our patent portfolio is one of our finest assets. The Phase 1 clinical programs in INKmune are being run in the UK.

The UK is suffering mightily from the COVID-19 pandemic, as are we. And both programs have been somewhat delayed by the fact that, you know, they aren't allowing clinical trials to move forward because of the pressures on the hospital.

We are cautiously optimistic that we can meet our goal to treat a patient within the high-risk MDS program by the end of the year. Realistically, we do not expect to treat a patient in the INKmune ovarian cancer trial until the first half of 2021.

So with that, I will turn it over to David who will talk about financial results, and upcoming milestones..

Thank you, RJ. I'll provide a brief overview of our financial results and upcoming milestones. Net loss attributable to common stockholders for the first quarter ended March 31, 2020, was 2.1 million compared to 1.9 million for the quarter ended March 31. 2019.

Research and Development expenses total approximately 0.8 million for the first quarter ended March 31, 2020, compared with approximately 0.6 million for the quarter ended March 31, 2019. General and administrative expense was approximately 1.3 million in each of the quarters ended March 31, 2020 and March 31, 2019.

At March 31, 2020, the company had cash and cash equivalents of approximately 5.9 million with no debt. As of May 13, 2020, the company had approximately 10.8 million shares outstanding. Now, I'd like to list our upcoming catalysts.

To reiterate what we have detailed in our press release, some of the milestone timelines have been updated due to the ongoing COVID-19 pandemic as RJ just spoke about.

First, we expect to report the results of the ongoing Phase 1 XPro1595 trial and Alzheimer’s disease expected to be completed in the second half of 2020 and half date in October, possibly sooner. Second, we expect to submit an IND for Quellor for the prevention of pulmonary complications of COVID-19 infection this month 2020 or very early next month.

Moreover, we are working to enroll the first patient in a phase two Quellor program, as soon as possible. Third, we expect to enroll the first patient in the Phase 2 INB03 program targeting trastuzumab resistant HER2+ breast cancer using INB03 as part of combination therapy in mid-2021.

Fourth, we expect to enroll the first patient in Phase II LIVNate for NASH in mid-2021. Fifth, we expect to enroll the first patient in Phase I INKmune in High Risk MDS cancer by the by the end of this year in the second half of 2020. Sixth, we expect to enroll the first patient in the Phase 1 INKmune even program in ovarian cancer by mid-2021.

So, as a small company, we have a lot of catalysts coming up. We remain very focused on meeting our milestones and delivering data and rewarding investor’s faith and patience in the development of our business. 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 questions and answers.

[Latania,] can you please poll for questions..

Thank you. [Operator Instructions] Our first question comes from Jonathan Aschoff with ROTH Capital Partners. Please proceed with the question..

Thank you. Hi, guys. I have two questions.

The first is, since Lapatinib is the drug with which you intend to combine DN-TNF with Phase II, can't it be argued that that drug has kind of already had its heyday and therefore maybe restoring Lapatinib sensitivity isn't as commercially exciting as restoring trastuzumab sensitivity? You want to discuss that a little?.

Yeah, that's a great question, Jonathan. The problem is, is that once you get down to the way clinicians treat patients.

Once the patient has failed a drug, once they relapsed basically on trastuzumab, which is what happens when a patient develops metastatic disease, particularly brain mets, they move on, right? And to argue to go to a, it's a difficult discussion frequently to have with clinicians, when they say, to say, well, we can now – if you give Lapatinib, let's say you give Lapatinib with trastuzumab, the patient's going to respond.

They get nervous about that, but let's talk – let's really take the next step. Obviously, there are a number of these trastuzumab drug conjugates out there now, and some of them have been – has shown a bit of a signal in the brain.

The problem is with a trastuzumab based conjugate is if the patient is expressing MUC4, which almost all of these metastatic patients do, in fact, the trastuzumab can’t bind to HER2.

So, actually, trastuzumab resistance is actually a, you know, shall we say a biomarker for resistance to any trastuzumab based strategy? So, I think you're – I think, I actually think the future and I'm speculating here is that I admit Lapatinib has, you know, maybe it had its day in the sun, but it is indicated for the indication and there are other PKI’s that shows some that are newer, that shows some signal in these indications.

I just don't have data, which I predict in the future that will be combining INB03 with a number of PKI’s because this may be a class effect. I don't know that yet. It may be. We are doing that research, but we have indications that that might be the case. So, I accept your comment, but it's hard to go against tradition.

The tradition is once a clinician – once a patient has progressed on a therapy, they move on..

Okay, what questions will be [more dear headed]? Can you help us, David better understand the quarterly R&D expense trend over 2020, just looking at the drop from 4Q to the first quarter?.

I'm sorry, Jon, you want the R&D expense going forward?.

Yes, yes, just because there was such a big drop from the fourth quarter of 2019 to the first quarter of 2020..

I'll tell you what, we're currently evaluating the costs related to the COVID trial. It's somewhere the first part of the trial be somewhere between 3 million to 5 million. We're looking at non-dilutive activity related to that. We're also looking at whether we can run what percentage of the trials we run in Australia, which allow us to get a rebate.

I would like to take that offline with you, if you don't mind, Jonathan and have a call with you about that after this, if you don't mind..

No problem. That's all I have. Thank you..

Our next question comes from Jason McCarthy with Maxim. Please proceed with your question. Q - Jason McCarthy Hey, guys, thanks for taking the questions.

Can you talk a little bit about the amount of drug product that you do have manufacturer, you mentioned it earlier? And how much of that would be applicable to a COVID study and for that COVID study, you know, can you walk us through a little bit of what you're thinking in terms of a trial size and maybe stage of disease would it be severe/ICU intubated or something more mild-to-moderate or something in the middle, maybe in the hospital, but not in the ICU just yet, just a little bit more clarity there.

And a question for David, on the back end of that would be, can you just elaborate a little bit on your relationship with KBI Pharma, because they, they are a great manufacturing partner. They support coherence and a bunch of other names. This talk a little bit about drug manufacturing with KBI..

Yeah, so let me start.

So, we have, you know, we have more than enough drug to complete the COVID trial and the Alzheimer’s trial, but we don't have enough drug to really jump into another trial that may have extensions and what I mean by that, when you set up a trial, for instance, a cancer patient, and if the patient's doing well on the therapy, the expectation as you carry them, you continue to treat them under the end of the trial.

So, we cannot make open end commitments. The COVID trial is an interesting trial. When we talk to the FDA, we sent in one design and they brought push back and actually with a better design.

They are asking us to do a two-step Phase 2 trial that is, they want 100 patient proof-of-concept that will ride into a fully powered – for all practical purposes pivotal trial that will allow us to really sit with the FDA and see what the next steps are. The way we've designed it.

So, the 100 patients is a randomized blinded trial, one-to-one randomization. The follow on trial is 260 patients so a total of 360 patients will be treated one to one with that no go decision after the first 100 patients.

The target patient is a patient who is admitted to the hospital with hypoxia, a [indiscernible] less than 94%, but not someone who's in the ICU.

The purpose of the trial is to keep the patient out of the ICU and the primary endpoint, and once again, this was dictated by the FDA is respiratory failure and we define respiratory failure as progression to mechanical ventilation, which is anything that has a ventilator with a plug attached to it.

So CPAP, BiPAP and traditional intubation with mechanical ventilation are the endpoints and part of the reason is, as you know, there's been – there's a really rapid change about how people are using intubation, people are using non-endotracheal tube forms a ventilation as long as they can, but our goal is to take a patient who comes it.

May need oxygen support, and keep them from sliding down that slippery slope. We are very interested in the other pathologies with COVID-19. I mentioned the endothelial activation, which is, I think, underestimated in the disease.

It is the cause of the coagulopathy, which contributes to the renal disease, it contributes to neurologic complications, and is actually probably a big part of the problems before they develop the more traditional form of ARDS. The patients we're treating will not have ARDS. It's not that we don't think the drug is a good drug for patients in ARDS.

It's just that that's, in my opinion, a different patient population. And we – I'd rather keep – I've taken care of those things. They are difficult patients, and I'd rather keep patients out of the ICU off mechanical ventilation, than try to wrestle them once they've gone that far. So, I'll stop there.

And let David answer the question and then let you respond, Jason..

Jason, thanks for the question. Yeah, we signed an agreement with KBI. They're a wonderful group. We've had a lot of discussions with them and we have a very good consultant that we use as an intermediary to help us on the manufacturing front. We actually run this through our UK sub, so it's eligible for a rebate from the UK Government.

It's somewhere between you know, it's, it'll be a long term relationship because as this – if this goes well, obviously we'll need to continually manufacture drug as the programs expand, but the first part of the – it's broken into really two different phases, and the first phase is really to do a pilot scale manufacturing and then the second phase is to do the clinical grade material manufacturing.

We estimate it's about a 14-month, 14 to 18 month type period of agreement. Could be accelerated, could be, but it's a great arrangement that we have with them..

Okay, great. And where would the trial be conducted? Would you be in Australia or someplace ex-U.S.

where you get rebates? I thought I recall Australia was one of your site?.

Well, it was. I tell you, I was interested because as you know, we love the rebates right. It's been a great source of [indiscernible], but if you've been – if you've happen to, you know, like I do, look at their Australian government website, they have done an extraordinary job of squashing the curve.

I think two days ago, they had 80 patients in the hospital and 40 in the ICU, and that was on the whole country wide. So, this trial will be run primarily in the United States, and I will say one of the other areas, we're very interested in, as you know, that Blacks and Hispanics have a rough go of it with this disease.

And there's a big debate about whether this is because of they have, you know, more of the comorbidities or if there's something else going on.

So, you know, I predict we will be running this in, you know, the centers or the parts of the country where the disease tidal wave is starting to hit, you know, places in the Mid South, Texas, the Southwest, and the Southeast.

And we plan and hope to have a patient population that looks a lot like the box, you know, a third Caucasian or a third Hispanic and a third Black because when you're treating almost 400 patients, you can really learn a lot from them. But, you know….

Is the fall season coming in Australia? Is that a possible factor for not having a few cases? Are you watching that? Or….

Oh, yeah, we're watching that, but I think the problem, there's really a couple of issues there. One, what's happening there about to start the influenza season.

So, what's going to happen is the same thing that's going to happen here as they begin to open up, they're going to have spots of disease, right? And they're going to see more cases than they see now, but the question is, are they going to have the kind of intensity where you can pick three or four hospitals and pick up enough patients? It's a moving target really, Jason.

I am not ruling out having sites in Australia, but the trial will be driven for the most part, assuming things work out with the IND and the FDA. The patient enrollment will really be driven out of the U.S..

Okay, perfect. Thanks for taking the question..

Our next question comes from Michael Erwin with Universe Securities. Please proceed with your question..

Hi. I actually have a few questions.

So, you said before that there was going to be some pushback of the trials for some of your plans [indiscernible] start later this year, are there any, you said before that you would release more data, but is there more information about the clinical design? Are there any plans of [exceeding] the results for those trials to make up that one year delay?.

Well, certainly the – no. Once we start the trial, the trial design is fixed. I mean, at the end of the day, as you know what the limiting factor to almost every trial is, speed of enrollment. So, at this point, you know, they are just being reset, to move back to reflect the pandemic. .

Okay, and then there's been news online about this complications with COVID-19 showing in pediatrics of a Kawasaki-like disease, and are there any plans of looking into this because there are some small links between TNF inhibitors and treatment options for Kawasaki disease?.

Actually, we are – thank you for that question. We're following that very closely. You are absolutely right. There is a role for – a big role of TNF in the Kawasaki syndrome that – in Kawasaki’s disease, and we expect that there's a similar role in this multi-system, this pediatric multi-system, inflammatory disease, I believe that's the name.

So, we've not yet seen anyone publish cytokine data. We're looking for that very closely. We expect it's going to model what we see in Kawasaki disease.

One of the things that the FDA made very clear in their response to us for a pre-IND, and actually in the guidance they just released on Monday for clinical trials and COVID-19, is that you need a pediatric plan, and although they don't hold you hostage to that plan, do you have to have that plan very quickly.

Right now, we view that disease as our potential pediatric plan. I emphasize potential, we've not discussed it with the FDA yet.

And we await to get a little – see some data to further support our interest, but once that our IND assuming everything goes well is open, and we start having follow-on discussions with the FDA, this is a disease that we think we have the perfect drug for because remember, it targets TNF.

The targets endothelial cell activation, which is a big part of this disease, and it is not immunosuppressive and one of the major differentiators of our anti-inflammatory strategy for many others out there is that we do not cause immunosuppression. In fact, we improve the immune response.

We have been – if you give animal models that have bacterial infections or protozoal infections they get better. We have tested this drug in models of Eastern Equine Encephalitis and in Coxsackie B3 with the NIAID and we did not make those animals worse. They did not die faster. We didn't make them get better, either but we did not.

They did not go worse. So, this drug is not immunosuppressive, which is an important consideration when you're treating people that have viral disease..

Alright, that's everything I got. Thank you very much..

[Operator Instructions] Our next question comes from Arthur He with H.C. Wainwright. Please proceed with your question..

Good afternoon, RJ and David. Thanks for taking my question. It is Arthur for RK. Most of my question be answered. I just have two – maybe two quick ones. So, first one for only your COVIDF-19 program, if I recall correctly you expect to start the trial in July.

Could you give us more color on your expectations for the – overall timing of the program?.

Yeah, so good question, you know, so obviously the calculation of July is, you know, obviously depends on the FDA. And I want to give, you know, I'm sure you've heard this from other companies, the FDA has been spectacular in dealing with the COVID-19 issue. They are quick in their responses. They're clear.

They are here to help, which is often not the way it seems when you're a small biotech because they can be a rough taskmaster. The rate of enrollment, obviously, it would depend completely on where the disease is in the US.

I think that anyone who thinks the disease is going to disappear in the summer, there are few people that do, I'm not one of those people.

As I mentioned earlier, I think it's going to roll you know, I think it's going to roll across the South and the South Central in the Midwest, and then in the fall we’re probably going to have secondary outbreaks where the first outbreaks are in the Wayne, the east coast and the West Coast. I think it's going to be here for a while.

The current plan is that we're going to, for the 100 patient go-no-go is five to seven sites. And the assumption is that they'll enroll at least one patient a week. So, you can do the math. It’s a 100 patient randomized trial, 50 get drugs and 50 don't get drugs.

By the way, David, I forgot to add, talk about the way that the dosing when Jason asked, but the – and this is actually the FDA’s recommendation, by the way. We designed it as a two-dose study on a mission and seven days later, and they pushed back and said, make it a one dose study with a second dose if they are in the hospital.

The expectation or the hope is that most of these patients actually leave the hospital by seven days. So, to treat the 360 patients that we need to treat since only half of those or 100, you know let’s call it a 180 patients are getting treatment. And let's say 20% get more than two doses.

I mean 250 viles is all we need for this clinical trial, 350 dose – 250 doses. So, that's a very – it’s a beautiful thing when you're a company doing a drug study where the drug supply is not a tremendous burden.

But anyway, Arthur, back to your question, our hope is, you know, the speed of which the trial enrolls is completely dependent on how severe the disease is. We will be placing our sites where we think the disease is going to be active this fall, this summer and fall..

Okay, thanks. Thanks for like color.

And just the one question on the Alzheimer’s disease program, could you remind us the - what's the beta [said weeks], but could expecting later this year?.

So remember, just a reminder, this is a Phase I trial in patients with inflammation and Alzheimer's disease and so they had to have inflammation, biomarkers of inflammation to be enrolled because remember, we're – our hypothesis is that neural inflammation is a cause of their disease. So, they get treated for three months.

And the primary readouts, the primary goal of the trial is to prove we get rid of neural inflammation.

The hypothesis is, is that if neural inflammation causes, you know, nerve cell death and synaptic dysfunction, if we get rid of neural inflammation, then we will improve – decrease the amount of nerve cell death and synaptic dysfunction, but to get a cognitive readout is going to take more than three-months.

So, we are getting all that cognition, assay or not assays but measures, but that's not the primary endpoint. The primary endpoint is four different buckets. We have inflammatory and neurodegenerative biomarkers and bloods and CSF. So, you know, cytokines, neural filament.

We're using the Roche neural toolkit for these assays, so that's blood and CSF is standard. We are measured using MRI imaging to look at white matter free water, which is an area that I am quite keen on. It turns out that neural inflammation increases the amount of free water in the white matter and you can measure that by MRI sequences.

So that is a very attractive biomarker that we are getting a breath test looking at volatile organic compounds that are expressed in the [breath], which is an excellent biomarker of inflammation. And then finally, we are looking at what we call the behavioral biomarkers.

It turns out that depression, agitation, hallucinations, sleep disorders, and apathy are common problems in Alzheimer's patients and they are exquisitely sensitive to neural inflammation. So, the assumption is or the hypothesis is that these will improve. So, it's this suite of five biomarker buckets that we're looking at.

And that is the, those are the endpoints that we're going to use to move into Phase II..

Great, thank you. Thank you for that. And just one maybe quick housekeeping question for David.

So, regarding the SG&A expense line, could [assuming] goes flat over the rest of the year?.

Yes, yes, you can, Arthur..

Okay, great, thank you..

At this time, I would like to turn the call back over to Mr. RJ Tesi for closing comments..

So, we'd like to thank you all for joining us today. We are excited about the future. As you know, we have a full plate or full slate of programs. We are working hard in these difficult times. We have prioritized our programs in a way that we think we can bring value to the company and to investors and to make a difference at the bedside.

So, with that, I thank you all, David, anything you want to add?.

No, I appreciate everybody's patience in what we're doing here and I certainly appreciate everybody's support. And as with always, if you have questions, please reach out to us individually and independently, we'd be more than delighted to chat with you..

Thank you. This does conclude today's teleconference. You may disconnect your lines at this time and have a great day..