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Reduces Amyloid and Enhances Behavior Post Traumatic Brain Injury in an Animal Model of Alzheimer's Disease: Supported by Department
Treatment Post-TBI Prevents Short- and Long-Term Alzheimer's-like Pathology in transgenic mice
Raton, Florida, June 10, 2025 (GLOBE NEWSWIRE) -- INmune Bio, Inc. (NASDAQ: INMB) (the "Company"), a clinical-stage
inflammation and immunology company focused on developing treatments that harness the patient's innate immune system to fight disease
is collaborating with Kirsty Dixon PhD, Assoc Prof. of Surgery at Virginia Commonwealth University in Richmond, Virginia on the interaction
of TBI and AD. Prof Dixon and her team presented a poster at the Keystone Symposia's Neurodegeneration section: Linking Cellular
Pathways to Therapeutic Strategies in Whistler, British Columbia, Canada. The poster demonstrates that Traumatic Brain Injury (TBI) increases
amyloid deposition in high-risk animals and that administration of XPro (XPro1595, pegipanermin) significantly reduces
amyloid formation and improves clinical measures of brain function.
Brain Injury is a well-established risk factor for Alzheimer's disease (AD). TBI promotes neuroinflammation, increasing the inflammatory
cytokine Tumor Necrosis Factor (solTNF), which has been implicated in AD progression. A key protein in AD pathogenesis is the enzyme
-secretase (BACE1), which cleaves amyloid precursor protein (APP) to generate neurotoxic amyloid beta (A 42), potentially
leading to neuronal loss. Under pathological conditions, TNF receptor 1 (TNFR1) upregulates BACE1 and cell death pathways. Therefore,
targeting TBI-induced solTNF/TNFR1 signaling may mitigate A 42 production and neuronal loss, providing a critical translational
link between TBI and AD.
study showed that TBI triggered a transient increase in TNFR1, BACE1, and A 42 expression in the hippocampus, peaking three days
post-injury and returning to baseline by day seven. Administering XPro thirty minutes post-injury inhibited solTNF/TNFR1
activity and prevented elevations in TNFR1, BACE1, A 42, and caspase-3 levels. Immunofluorescence revealed that XPro treatment
reduced intracellular neuronal amyloid accumulation in the hippocampus and improved neurological outcomes in treated animals.
findings demonstrate that TBI exacerbates amyloidogenesis and behavioral deficits in the hippocampus through solTNF/TNFR1 signaling,"
said Dr. Dixon. "These results support XPro as a promising treatment to reduce AD pathology risk post-TBI and elucidate a key cellular
mechanism linking inflammation to neurodegeneration." A collaborator to the study Elliott Mufson, PhD, professor of neurobiology,
the Greening Chair for Neuroscience Research, and the director of the Alzheimer's disease research laboratory at Barrow Neurological
Institute said, "An important feature of these findings is that XPro targets neurobehavioral dysfunction resulting from brain trauma
and age-related neurodegenerative disease, which holds great promise for people suffering from these disorders."
brain injury from falls is a significant concern for the elderly population at risk for Alzheimer's disease, as it accelerates
dementia onset," said RJ Tesi, MD, CEO of INmune Bio. "Effectively treating the resulting CNS pathology is critical to preserving
cognitive function in this vulnerable group."
Number: 2537 Session: Poster Session 2: 6/10/2025
Neurodegeneration: Linking Cellular Pathways to Therapeutic Strategies;
Poster Title: TBI-induced solTNF/TNFR1 exacerbates Alzheimer's disease pathophysiology and neurological deficits
Authors: Chelsie N. Poffenberger, Subrat Poudel, Michelle M. Taylor, Elliott J. Mufson, Kirsty J. Dixon
is a next-generation inhibitor of tumor necrosis factor (TNF) that is currently in clinical trial and acts differently than currently
available TNF inhibitors in that it neutralizes soluble TNF (sTNF), without affecting trans-membrane TNF (tmTNF) or TNF receptors. XPro
could have potential substantial beneficial effects in patients with neurologic disease by decreasing neuroinflammation. For more information
about the importance of targeting neuroinflammation in the brain to improve cognitive function and restore neuronal communication visit this section of the INmune Bio's website.
a publicly traded (NASDAQ: INMB), clinical-stage biotechnology company focused on developing treatments that target the innate immune
system to fight disease. INmune Bio has three product platforms: the Dominant-Negative Tumor Necrosis Factor (DN-TNF) product platform
utilizes dominant-negative technology to selectively neutralize soluble TNF, a key driver of innate immune dysfunction and a mechanistic
driver of many diseases. DN-TNF product candidates are in clinical trials to determine if they can treat Mild Alzheimer's disease,
Mild Cognitive Impairment and treatment-resistant depression (XPro ). The Natural Killer Cell Priming Platform includes INKmune developed
to prime a patient's NK cells to eliminate minimal residual disease in patients with cancer and is currently in trials in metastatic
castration-resistance prostate cancer. The third program, CORDStrom , is a proprietary pooled, allogeneic, human umbilical
cord-derived mesenchymal Stromal/Stem cell (hucMSCs) platform that recently completed a blinded randomized trial in recessive dystrophic
epidermolysis bullosa. INmune Bio's product platforms utilize a precision medicine approach for diseases driven by chronic inflammation
and cancer. To learn more, please visit www.inmunebio.com.
Forward Looking Statements
trials are in early stages and there is no assurance that any specific outcome will be achieved. Any statements contained in this press
release that do not describe historical facts may constitute forward-looking statements as that term is defined in the Private Securities
Litigation Reform Act of 1995. Any statements contained in this press release that do not describe historical facts may constitute forward-looking
statements as that term is defined in the Private Securities Litigation Reform Act of 1995. Any forward-looking statements contained
herein are based on current expectations but are subject to several risks and uncertainties. Actual results and the timing of certain
events and circumstances may differ materially from those described by the forward-looking statements because of these risks and uncertainties.
CORDstrom , XPro1595 (XPro , pegipanermin), and INKmune are still in clinical trials or preparing
to start clinical trials and have not been approved by the US Food and Drug Administration (FDA) or any regulatory body and there cannot
be any assurance that they will be approved by the FDA or any regulatory body or that any specific results will be achieved. The factors
that could cause actual future results to differ materially from current expectations include, but are not limited to, risks and uncertainties
relating to the Company's ability to produce more drug for clinical trials; the availability of substantial additional funding
for the Company to continue its operations and to conduct research and development, clinical studies and future product commercialization;
and, the Company's business, research, product development, regulatory approval, marketing and distribution plans and strategies.
These and other factors are identified and described in more detail in the Company's filings with the Securities and Exchange Commission,
including the Company's Annual Report on Form 10-K, the Company's Quarterly Reports on Form 10-Q and the Company's
Current Reports on Form 8-K. The Company assumes no obligation to update any forward-looking statements to reflect any event or circumstance
that may arise after the date of this release.
Chief Financial Officer
Head of Investor Relations