INmune Bio DN-TNF Clinical Trial, Complications of Cytokine Storm Caused by COVID-19

DN-TNF Clinical Trial, Complications of Cytokine

Storm Caused by COVID-19

and Chief Medical Officer

John Aschoff - Roth Capital

Michael Carmia - BTIG

Jason McCarthy - Maxim Group

R.K. - H.C. Wainwright

Carl Byrnes - Northland Securities

Greetings, and welcome to INmune Bio's

Conference Call to discuss the company's DN-TNF clinical trial to determine if it will successfully treat the complications

of cytokine storm caused by COVID-19. At this time, all lines are placed on a listen-only mode, and the floor will be open for

questions and comments following the presentation. If anyone should require operator assistance during the conference, please press

star, zero on your telephone keypad. As a reminder, this conference call is being recorded. A transcript will follow within 24

hours of this conference call.

At this time, it is now my pleasure to

introduce your host, R.J. Tesi, CEO and Chief Medical Officer, and David Moss, CFO. David, the floor is yours.

Thank you, Devon, and good afternoon, everybody.

We thank you for joining us on--for the INmune Bio conference call to discuss our strategy related to COVID-19. As we have stated

before, we believe we have a unique drug in our DN-TNF platform that addresses complications of inflammation, and we know that

in the case of COVID-19, rapid hyperinflammation can cause a series of events that can lead to death. With me on the call is CEO

and Chief Medical Officer, R.J. Tesi, who will go into more detail about our clinical program related to COVID-19.

Before we begin, I remind everyone that

except for statements of historical fact, 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 risk 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 the risk factors in the company's SEC filing,

including in our most recent quarterly filing with the SEC.

Our DN-TNF platform is beginning trials

for the treatment of complications of cytokine storm, and 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 as law, INmune Bio disclaims any obligation to update these forward-looking

statements to reflect future information (SP), events, or circumstances.

Now, I'd like to turn the call over

to R.J. Tesi, the CEO of INmune Bio. R.J., please proceed.

Thank you, and thank you, everyone, for

joining us. And just on a personal note, if you see a health care worker who has been on the front lines, give them your hearty

thanks. They deserve it.

COVID-19 has consumed us all for the last

two months, particularly those of you in New York. You just can't get away from it. It's been a pretty remarkable period

of time. The pathology is driven by the cytokine storm, which is an uncontrolled, disregulated, and sometimes lethal, inflammatory

response, primarily driven by the innate immune system. The pro-inflammatory cytokines of IL-1, 6, and soluble TNF are elevated

in patients who are hospitalized, and these are the main culprits in the cytokine storm of COVID-19. INmune Bio is the inflammation

company focused on the innate immune system. We have a dog in this fight.

So, how did we get here? We signaled during

our end-of-year conference call on March 11 that we were in the midst of a strategic analysis to determine if and how INmune Bio

should get involved to help with the current pandemic. We did a careful scientific review. And I have to say any of you that have

been following this pandemic know that the medical community has just been remarkable in the amount of data that has come out from

places like China and Europe and beyond.

We assess the clinical need and consider

the realities of financing and initiating a clinical trial in the midst of a pandemic. I will talk more about these in a moment.

To be clear, our program is not a vaccine. We're not an antiviral program that kills virus. DN-TNF should decrease the severity

of the inflammatory pathology associated with the viral infection. That is what we are planning to do.

So, what is the scientific evidence that

says we should be going down this road? Soluble TNF is one of the cytokines that is elevated in patients with COVID-19, and it's

part of the cytokine storm that is really the cause of much of the medical morbidity and mortality associated with the virus. I

remind you that I'm talking only about soluble TNF. Any TNF that you hear about, read about, in the papers is soluble TNF.

They are not talking about transmembrane

TNF, which, as you recall, is the good TNF. They are not talking about TNF receptors, which are really not that important in this

disease at this point. We are the only ones that have a targeted agent that only affects--neutralizes soluble TNF that has advantages--may

have advantages--in both biology, safety, and therapeutic breadth. We talk about this all the time. Please go to our website to

Soluble TNF plays actually two roles in

the inflammatory response associated to COVID-19. The obvious role is that it activates immune cells, and the immune cells cause

the inflammation and the tissue damage that promulgates the--the disease. The less obvious role is that soluble TNF activates endothelial

cells. Endothelial cells express ICAM-1 and--and VCAM-1, which are proteins that signal the leukocytes in the blood to marginate

then migrate through the blood vessel wall to the tissue, where they cause damage.

Put simply, soluble TNF brings the wood

to the fire, and it supplies the match to light it. We think this double whammy is important. And endothelial activation is now

being discussed more as the disease--as the threat of not enough ventilators has passed. And this hypercoagulable state, the problems

with renal failure and the problems with increased cardiovascular risk, are probably all associated with this endothelial activation.

So, is DN-TNF the right drug? We believe

the answer is yes for three reasons: the mechanism of action of the DN-TNF aligns well with the pathophysiology of cytokine storm;

it is not immunosuppressive--and I'll come back to that; and it is very easy to use, something that's very important

in the chaos of a surge.

We have been preaching for more than two

years that DN-TNF neutralizes soluble TNF, and the soluble TNF levels in COVID-19 patients can reach 100 picograms per mL. That's

more than 10 times the level that you and I have sitting here, assuming none of us have COVID-19. We know from the data from our

oncology Phase I trial that stable trough levels of DN-TNF in the blood are achieved such that it will neutralize more than 99.9

percent of TNF in the patient's blood, even at those very high levels of 100 picograms per mL. The risk of overshooting is

low because the drug is well tolerated. If someone only has 50 picograms per mL, nothing is lost.

Will--will DN-TNF therapy affect cytokine

storm? We believe the answer is yes. IL-6, Il-1, and soluble TNF are elevated in the cytokine storm. We always preach that soluble

TNF is the master cytokine that drives the expression of IL-6 and IL-1. They are located downstream of TNF translation. And data

from our oncology Phase I confirm that when we neutralize soluble TNF in these patients, their IL-6 levels go down.

Finally, there are anecdotal points--reports--that

if you treat one inflammatory cytokine of the cytokine storm--in this case IL-6--there are a number of anti-IL-6 trials in place--the

patients with acute respiratory distress syndrome appear to get better. I will emphasize they are anecdotal reports at this point.

But, safety is key. Any therapy that is used to treat patients with COVID-19 must not make the patient worse. Above all, do no

I was a transplant surgeon in a previous

life, and I spent years treating immunosuppressed patients with life-threatening viral infections. I have hard-won experience in

this area. And anti-inflammatory strategies must cause no harm. And there aren't many that exist that are not immunosuppressive.

The clinical reports from Wuhan and the

World Health Organization, WHO, are in agreement. Corticosteroids increase the mortality of patients with COVID-19. According to

FDA labeling, the existing anti-IL-6, anti-IL-1, and anti-TNF therapies are contraindicated in patients with ongoing infection.

DN-TNF is not immunosuppressive, and mirroring (SP) models of cancer and bacterial infection, DN-TNF improves the immune response.

We have studied DN-TNF in models of viral infection. DN-TNF does not compromise the immune system to the virus.

Last--last year we worked with NIAID to

study the effects of DN-TNF in animal models of EEE--that's eastern equine encephalitis virus--and coxsackie B3 virus. And

in these infected animals, DN-TNF did not affect mortality, nor did it affect in the case of coxsackie B3 tissue invasion, the

virus. These data are not yet published, but the official reports have been included in the document sent to the regulatory authorities