Full Press Release Details
C O R P O R A T E P A R T I C I P A
David Moss, Chief Financial Officer,
Treasurer & Secretary
RJ Tesi, Co-Founder, President,
Chief Executive Officer, Chief Medical Officer & Chairman
C O N F E R E N C E C A L L P A R T
Jonathan Aschoff, ROTH Capital
Julian Harrison, BTIG
Jason McCarthy, Maxim Group
Michael Irwin, Univest Security
P R E S E N T A T I O N
Greetings and welcome to the INmune Bio
Third Quarter 2020 Earnings Call.
During the presentation, all participants
will be in a listen-only mode. Afterwards, we will conduct a question-and-answer session. At that time, if you have a question,
please press the one, followed by the four on your telephone. If at any time during the conference you need to reach an Operator,
please press star and zero. As a reminder, this conference is being recorded. A transcript will follow within 24 hours of this
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, Kevin, and good afternoon, everyone.
We thank you for joining us for the call of INmune Bio's third quarter 2020 financial results. With me on the call is Dr. RJ Tesi,
CEO and Co-Founder of INmune Bio, who will provide a business update.
Before we begin, I remind everyone that
except for statements of historical fact, 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. 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.
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There is no assurance of any specific outcome.
Undue reliance should not be placed on the 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, 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 Dr.
RJ Tesi, Co-Founder, CEO of INmune Bio. RJ?
Thank you, David, and thank you, everyone,
for joining the call. I will arrange my remarks to highlight key takeaways for the third quarter, year-to-date and provide updates
on our two platform programs, before I pass it back to David to discuss our financial results and upcoming milestones. Then we
I'll start with our DN-TNF program, beginning
with XPro1595, which we are developing for Alzheimer's disease and other CNS indications where neuroinflammation plays an important
role. A significant highlight since our last quarterly update was the announcement in September that we were awarded a $2.9 million
SBIR grant from the NIH to support a Phase 2 study in XPro1595 in patients with treatment resistant depression. In rough numbers,
we expect to receive $0.75 million this year, $1.2 million in 2021 and the balance in 2022. Importantly, we will conduct this trial
in collaboration with two of the world's pioneers in this field, Professor Andrew Miller, MD; and Associate Professor, Jennifer
Felger, both at Emory University.
Treatment resistant depression is an indication
with a significant unmet need. An estimated 7 million patients in the U.S. with major depressive disorder are resistant to current
therapies. The definition of treatment resistant depression is simple, the patient must fail two lines of treatment for their depression
to be labeled treatment resistant. There are two surprises hidden in that simple statement. The diagnosis is one-that one
comes to by trial and error of treatment. There are no biomarkers that predict which patients are going to be successful or fail
or which drug you should use.
Imagine a disease with 7 million patients
is treated with the diagnostic precision of some ancient time, namely hit and miss. I find that remarkable. This trial hopes to
change that, at least to begin the process of changing that. The trial will use biomarkers of inflammation to enroll patients and
will use biomarkers to determine responsive therapy with XPro, a strategy that is rarely, if ever used, in the development of psychiatric
drugs. Based on our work using XPro to treat patients with neuroinflammation in Alzheimer's disease, we believe treatment with
XPro will decrease neuroinflammation in the patients with treatment resistant depression; restore functional connectivity in a
reward-related brain circuitry, an MRI neuroimaging biomarker that can be seen; and will improve anhedonia, an important symptom
of major depression which is sort of apathy and they just can't get excited about anything.
A more detailed discussion of this biology
in the trial are beyond the scope of this call. I refer you to our September 29 KOL webinar that is posted on our website. Needless
to say, we are excited about the expansion of our neuroinflammation franchise beyond Alzheimer's disease and look forward to commencing
enrollment of this trial in 2021.
Turning to our flagship program in Alzheimer's
disease. In July, we presented interim data from a Phase 1 trial using XPro1595 to treat neuroinflammation in patients with Alzheimer's
disease. XPro reduced neuroinflammation by an average of 40.6% in a white matter pathway, important for language and memory in
patients with Alzheimer's disease. In this study, neuroinflammation is assessed in many ways, but as part of this preliminary data
snapshot, we focused on MRI measures of white matter free water, a validated biomarker of neuroinflammation.
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In the admittedly small preliminary data
set, we had six patients, half in a low-dose and half in a high-dose cohort-excuse me, that were treated for 12 weeks. As
a reminder, this trial is a neuroinflammation trial in Alzheimer's disease-in patients with Alzheimer's disease. The primary
endpoint is decreasing neuroinflammation. We are measuring cognitive changes but as in a 12-week trial, the expectation for significant
changes is tempered.
There were several important findings in
this preliminary data set. First, neuroinflammation was decreased over the 12-week period as measured by white matter free water.
White matter free water was measured in two ways: a whole brain measure using a white-safe white matter mask and we look
at neuroinflammation in specific white matter tracts, the super highway of the brain-connecting parts of the brain.
Using the safe white matter mask, we saw
a clear dose response with an increase of 1.7% of neuroinflammation over a three-month period in the low-dose group but a decrease
of neuroinflammation of 2.3% in the high-dose group. In a more detailed analysis of white matter tract pathology, we showed the
40% reduction of neuroinflammation in the arcuate fasciculus in patients treated with XPro. Every patient had a decrease and the
range was between 20% and 50%.
Why do we believe a decrease in neuroinflammation
in the arcuate fasciculus is important? The arcuate fasciculus is a major white matter tract that connects regions of the brain
important for language and short-term memory. Language, more specifically the deterioration of language skills, is a sensitive
clinical sign used by clinicians in Alzheimer's disease. Language skills or the deterioration of language skills are helpful in
the diagnosis of MCI, to monitor the progression of MCI to Alzheimer's disease and to measure the worsening of cognitive decline.
We acknowledge these are preliminary data
in a small number of patients. Regardless, we are encouraged by these results for three reasons. First, the results are predicted
by preclinical studies. Second, we treated Alzheimer's patients with a novel therapeutic protein by subcutaneous injection in the
thigh or abdomen like an insulin shot to decrease neuroinflammation in a specific nerve anatomic structure that is important in
one of the most sensitive clinical science of Alzheimer's disease, language. We believe this gives us considerable optimism.
Finally, we-in measuring white matter
free water using a sensitive, and I stress, noninvasive biomarker, that we will increase the precision and decrease the risk of
drug development in Alzheimer's disease and the other neurodegenerative diseases we will be looking to in the future. We look forward
to expanding the data set in the patients of the Phase 1 trial and studying patients who have entered the extension trial. The
extension trial is patients who reached their three-month deadline or treatment end-of-study and want to stay on the drug. They