Full Press Release Details
A T E P A R T I C I P A N T S
David Moss, Co-Founder and Chief Financial
Raymond (R.J.) Tesi, MD, Co-Founder,
President, CEO, Chief Medical Officer and Chairman
Christopher (C.J.) Barnum, Director
Mark Lowdell, Co-Founder, Chief Scientific
Officer & Chief Manufacturing Officer
C O N F E R E N C E C A L L P A R T I C I P
Thomas Shrader, BTIG
P R E S E N T A T I O N
Greetings, and welcome to the INmune Bio Third
Quarter 2021 Earnings Call.
As a reminder, this conference is being recorded.
At this time, it is my pleasure to introduce Mr.
David Moss, Co-Founder and CFO of INmune Bio. David, the floor is yours.
Good afternoon, everybody. We thank you for joining
us for the call for the INmune Bio's Third Quarter 2021 Financial Results. With me on the call is Dr. R. J. Tesi, CEO and Co-Founder of
INmune Bio, who will provide a business update on our DN-TNF platform; and Dr. Mark Lowdell, CSO and Co-Founder, who will provide an update
on our NK cell priming platform. We are also lucky to have Dr. C. J. Barnum, Head of Neuroscience, who will speak about our newly announced
Phase II program in Mild Cognitive Impairment, or MCI.
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 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 the risk factors in the Company's SEC filings, including our
most recently quarterly filing with the SEC.
ViaVid has made considerable efforts to provide
an accurate transcription. There may be material errors, omissions, or inaccuracies in the reporting of the substance of the conference
call. This transcript is being made available for information purposes only.
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There's 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 and as of the fact and
circumstances underlying forward-looking statements may change. Except as required by law, INmune Bio disclaims any obligation to update
these forward-looking statements to reflect future information, events, or circumstances.
Now I'd like to turn the call over to Dr. R. J.
Tesi, Co-Founder and CEO of INmune Bio.
Thank you, David, and thank, everyone, for joining
As is our practice, I will arrange my remarks
to highlight the key takeaways from the third quarter and subsequent period and provide updates on our platform programs. I will start
by reviewing our DN-TNF programs, then hand the call to C. J. Barnum, Head of Neuroscience for INmune Bio, who will speak about our new
Phase II program in patients with MCI, which is a prodromal form of Alzheimer's disease. Professor Mark Lowdell, our CSO, will speak about
recent developments with the INKmune platform before I pass it back to David Moss, our CFO, to discuss the financial results and upcoming
milestones. Then we'll move to Q&A.
XPro is our CNS platform. We have clinical programs
in Alzheimer's disease and treatment-resistant depression with IND-enabling studies underway in ALS. Each of these programs is supported
by extramural non-dilutive funding from the Alzheimer's Association, the NIH, and the ALS Foundation, respectively.
The common denominator of these CNS indications
is that neuroinflammation plays an important role in the disease. Neuroinflammation, however, is one step removed from the true pathology
underlying Alzheimer's disease. Those changes are loss of connections between neurons and nerve cell death. In the brain, neurons have
two parts. The cell body is in the gray matter and the myelinated axons are in the white matter. The first is where the memories are stored,
the latter allows neurons to communicate. Both are required for normal cognitive function.
Inflammation causes synaptic dysfunction, strips
axons of their myelin, and drives neurodegeneration of both axons and nerve cells. Put simply, neuroinflammation dramatically alters brain
biology precluding normal function.
INmune Bio believes that synaptic connections
can be restored and myelinated axons can be repaired with XPro therapy. INmune Bio is using novel technology to demonstrate the importance
of white matter pathology in Alzheimer's disease. The MRI biomarkers of white matter free water, apparent fiber density, and radial density,
measures of neuroinflammation, axonal integrity, and myelination, respectively, help locate and quantify white matter pathology, then
measure the effect of XPro therapy.
These powerful technologies provide new opportunities
for staging and treatment of CNS diseases and highlight the many effects of XPro therapy. The opportunities to use XPro beyond Alzheimer's
disease are real. More than 60 publications covering more than a dozen diseases gives a hint of the opportunities before us. These publications
can be found on our website.
We've given three webinars discussing the results
from the Phase I study of XPro in Alzheimer's disease patients. To summarize, treatment with XPro for three months decreases neuroinflammation,
decreases neurodegeneration, and improves synaptic function in patients with Alzheimer's disease. The last two benefits of XPro target
therapy that is the core pathology of cognitive decline, which is XPro, which is nerve cell death and synaptic dysfunction. In our opinion,
if a drug for AD does not improve one or both of these variables, there's little hope that the drug will make a difference in cognition.
Our data show that XPro improves both and does much more.
ViaVid has made considerable efforts to provide
an accurate transcription. There may be material errors, omissions, or inaccuracies in the reporting of the substance of the conference
call. This transcript is being made available for information purposes only.
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During the third quarter, we released additional
biomarker data that further supports our belief that XPro will make a different in patients with Alzheimer's disease. Much of the new
biomarker data is focused on white matter pathology. XPro improves multiple measures of white matter pathology. Unlike traditional volumetric
analysis of the brain, advances in MRI imaging allows us to measure the microstructural changes of specific white matter tracts as well
as axons and myelin within the white matter tract using techniques called apparent fiber density and radial diffusivity, respectively.
The concept of white matter tracts may be new
to you. White matter tracts our axonal superhighways that connects parts of the brain that must work together. There are many white matter
tracts, and not all are important in Alzheimer's disease. Our analysis is focused on the so-called seven AD white matter bundles. Those
are the white matter tracts most affected by Alzheimer's disease, and they include names like the anterior fasciculus, the frontal occipital,
corpus callosum and the cingulum, just to name a few.
The Phase I trial had two steps. All patients
were treated for three months, and six patients retrieved XPro for up to a year in the so-called extension trial. In the patients treated
for 12 months with XPro in the extension trial, there was continuous improvement in white matter volumetric changes in the temporal lobe
and increases in apparent fiber density and radial diffusivity within the AD bundles of 17% and 16%, respectively.
You may be thinking that doesn't sound like much,
but it is. To give perspective, over a 12-month period, apparent fiber density and radial diffusivity get worse in patients with Alzheimer's
disease. To our knowledge, improvement in these metrics has never been seen in patients. These observations or these improvements are
supported by data from the CSF protium that will be presented next week at CTAD, which is the big clinical trials Alzheimer's disease
meeting occurring in Boston.
We also observed an effect on XPro on more traditional
biomarkers of disease, specifically tau. Tau is a structural protein necessary for axon integrity. When phosphorylated, the axon degenerates.
Phosphorylated tau proteins are liberated from dying axons and can be detected in the CSF. The more phosphorylated tau present, the more
white matter loss is occurring. Of the many tau species, phosphor-tau 217 has the highest discriminative accuracy for Alzheimer's disease
and a strong correlation with amyloidosis and cognitive decline. When assessed in our patients treated with XPro for three months, CSF
levels of phosphor-tau 217 decreased 46%.
In summary, XPro improves the biology of brains
in patients with Alzheimer's disease. It decreases biomarkers of neuroinflammation and neurodegeneration while improving biomarkers of