Full Press Release Details
O R P O R A T E P A R T I C I P A N T S
Moss, Chief Financial Officer, Treasurer & Secretary
Tesi, MD, Co-Founder, President, Chief Executive Officer, Chief Medical Officer & Chairman
O N F E R E N C E C A L L P A R T I C I P A N T S
Aschoff, ROTH Capital Partners
Mamtani, B. Riley Securities
McCarthy, Maxim Group
Irwin, Univest Securities
Carlson, Tailwinds Research
R E S E N T A T I O N
and welcome to the INmune Bio First Quarter 2021 Earnings Call.
this time, it is my pleasure to introduce Mr. David Moss, Co-Founder and Chief Financial Officer of INmune Bio. David, the floor is yours.
you, Doug, and good afternoon, everyone. We thank you for joining us for the call of INmune Bio's First Quarter 2021 Financial Results.
With me on the call is Dr. RJ Tesi, CEO and Co-Founder of INmune Bio, who will provide a business update.
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 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
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.
1-888-562-0262 1-604-929-1352 www.viavid.com
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'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 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.
with the forward-looking statements behind us, I'd like to turn the call over to Dr. RJ Tesi, Co-Founder and CEO of INmune Bio. RJ?
you, David, and thanks, everyone, for joining the call. I will arrange my remarks to highlight the key takeaways for the first quarter
and provide updates on our platform programs before I pass it back to David to discuss our financial results and upcoming milestones,
then we will move to Q&A.
I did last quarter, I will begin today's call with XPro1595, which we are developing for Alzheimer's disease and other CNS indications
where neuroinflammation plays an important role.
our hypothesis, neuroinflammation results in synaptic loss and neurodegeneration, also known as nerve cell loss or death, in patients
with Alzheimer's disease. Nerve cells are where the memories are stored. Synapses are the wires that allow the nerve cells to communicate.
Cognitive decline can occur when nerve cells die, that is the memories are lost, or with synaptic dysfunction, that is the nerve cells
can't communicate with each other.
combination of synaptic dysfunction and neurodegeneration causes cognitive decline in patients with Alzheimer's disease. We believe that
for a drug to be effective in treating Alzheimer's disease, it must fix one or both of these pathologies. Based on data released so far,
XPro1595, the drug we are developing for the treatment of Alzheimer's disease, appears to improve both pathologies.
Alzheimer's program is all about targeting and controlling neuroinflammation with XPro1595. We believe neuroinflammation is a core pathology
of Alzheimer's dementia that must be controlled to treat cognitive decline.
the 23rd of January, we reported data on nine patients who had completed the full 12-week treatment period with XPro, three in the low-dose
group, and six in the high-dose group of 1 milligram per kilogram once a week as a subcutaneous injection. We expanded the data presented
from-that we had presented in July of 2020 to provide additional insight into the effects of XPro1595 in these patients with Alzheimer's
will focus on four highlights of that presentation. We demonstrated a highly significant correlation between measures of white matter
free water using MRI, with inflammatory cytokines in the CSF obtained by lumbar puncture. XPro caused both measures to decrease substantially
and significantly, suggesting that white matter free water may be a noninvasive measure of neuroinflammation that will spare patients
the need for an invasive lumbar puncture to sample CSF, and CSF is cerebral spinal fluid.
CSF proteome data provides hints to the benefits of controlling neuroinflammation with XPro. Highly significant decreases in neurofilament
1 and Visinin-like protein 1, both biomarkers of neurodegeneration suggests nerve cell death is decreased. Significant increase in synaptic
proteins, Contactin-2 and Neurogranin, demonstrate improved synaptic function. We presented an example of CNS remodeling in a patient
who, over nine months of weekly XPro treatment, had improvements in impaired fiber density, a novel measure of white matter quality,
and improvements in cortical disarray measurements, a novel measure of gray matter quality.
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.
1-888-562-0262 1-604-929-1352
we only showed one patient, this result was not unique. Eight of the nine patients reported in January were stable or showed improved
cognition over the three-month period, and the patients who responded with the greatest decrease in neuroinflammation had the greatest
improvements in measures of their cognitive performance during those three months. Of note, we presented the scans of white and gray
matter quality in a patient in that presentation. This patient was unique because we had the scan, but he had to quit his-or retire
from his work because his dementia was progressive. After six months of XPro therapy, he was able to return to work.
continue to follow these patients who are on the extension study and intend to provide further updates on their progress. I would encourage
you to review the KOL webinar from the January 21 presentation. It is available on our website. Also, all of what I've talked about is
available on a slide format in our nonconfidential corporate slide deck also found on our website.
find these results compelling. They clearly demonstrate that the treatment with XPro1595 when given as a once a week subcutaneous injection
for at least three months in patients with neuroinflammation with Alzheimer's disease have a decrease in that neuroinflammation. We remain
committed to starting a blinded, randomized, placebo-controlled study by the end of the year.
the meantime, we continue to generate data in our Phase I trial and in the patients who opted to stay on XPro in the extension study.
As a reminder, the duration of the Phase I study is three months. The patients can then opt to join an extension study that allows an
additional nine months of therapy. We have a handful of patients who have been on XPro for a year.
we report additional data from the Phase I this summer, we will provide data from new patients in the three-month study, additional biomarker
data in all patients, give insight into those who remain-who receive long-term XPro therapy in the extension study and provide
details of the Phase II trial design. Needless to say, based on our results to date, we are very excited about the future of this program.
remarkable attribute of XPro1595 is its ability to control neuroinflammation really cuts across a large range of neurodegenerative and
psychiatric diseases where neuroinflammation is a core pathology. What do I mean by that?
you're developing a drug that targets amyloid, you can really only treat Alzheimer's disease. With XPro1595, we can treat any CNS disease
where neuroinflammation plays an important role. That gives us a much bigger operating field. A current example is on the-is to
use XPro1595 for the treatment-for treatment-resistant depression. This Phase II trial is supported by a $2.9 million grant from
the Small Business Innovation Research administration associated with the NIH, and we will receive that money over the length of the
treatment-resistant depression market is substantial. In the U.S., an estimated 7 million patients suffer from TRD. The current treatment
paradigm involves a trial-and-error cycling through therapies to find one that works. A patient is labeled treatment resistant once they
have failed two regimens. This hit-and-miss approach is frustrating for patients and the clinical team and increases the cost of care.
That cost is substantial. It is estimated that the cost of treatment-resistant depression exceeds $64 billion a year to the U.S. health
care system. There is a real need for therapeutic advancements.
with the AD trial, we will use biomarkers of inflammation to confirm that treatment resistance is likely due to neuroinflammation. Once
the diagnosis is confirmed, patients are enrolled, treated for six weeks to determine response to XPro therapy.
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.
1-888-562-0262 1-604-929-1352
use of biomarkers is not routine in psychiatric drug development. We believe a precision medicine approach will make development of new
drugs for depression more efficient and will provide more effective therapies.
will conduct this trial in collaboration with two of the world's pioneers in the field, Professor Andy Miller, and Associate Professor
Jen Felger, both of Emory University. The six-week trial will be a double-blind, placebo-controlled study of XPro versus placebo, 45
of inflammation will be measured at baseline two and six weeks. The primary endpoint is improved functional connectivity measured by
MRI and reduction in biomarkers of inflammation. Secondary endpoints include clinical measures of motivation, which is the most sensitive
measure of-in patients with treatment-resistant depression. We are on track to begin this trial later this year.
is the name of the drug we used to treat patients in our COVID-19 program that targets cytokine storm in patients hospitalized with respiratory
compromise due to COVID-19. The double-blind, randomized, placebo-controlled trial is designed to enroll 366 high-risk COVID-19 patients
in two equal-sized cohorts. One cohort is a placebo plus standard of care, while the other is Quellor plus standard of care. The primary
endpoint is the need for mechanical ventilation or death during the 28 days following enrollment in the study.
secondary endpoints include transfer to the ICU, new onset of neurologic, cardiovascular, thromboembolic or renal disease. This summer,