XPro(TM) Reduces Amyloid and Enhances Behavior Post Traumatic Brain Injury in an Animal Model of Alzheimer's Disease: Supported by Department of Defense
MWN-AI** Summary
INmune Bio, Inc. (NASDAQ: INMB) has reported promising findings regarding its treatment XPro™ (XPro1595) in relation to Alzheimer’s disease (AD) and traumatic brain injury (TBI). In a collaboration with Dr. Kirsty Dixon at Virginia Commonwealth University, research presented at the Keystone Symposia revealed that TBI increases amyloid deposition—an AD hallmark—in susceptible animals. Administering XPro™ following TBI not only reduced amyloid formation but also improved neurological function in transgenic mice.
The study highlighted the role of TBI in exacerbating AD by promoting neuroinflammation via soluble Tumor Necrosis Factor (solTNF), which in turn upregulates ?-secretase (BACE1), an enzyme linked to the production of neurotoxic amyloid beta (A?42). The experiment demonstrated elevated expressions of TNFR1, BACE1, and A?42 in the hippocampus post-TBI, with levels normalizing within a week. Remarkably, XPro™ treatment initiated shortly after the injury inhibited solTNF activity and prevented the resultant biochemical and neurobehavioral deficits.
Dr. Dixon emphasized the significance of these findings, positioning XPro™ as a potential intervention to mitigate the risk of AD post-TBI. RJ Tesi, CEO of INmune Bio, pointed out the serious threat TBI poses to the elderly, especially given its association with dementia onset. XPro™, currently in clinical trials, represents a next-generation TNF inhibitor focused on reducing neuroinflammation without compromising beneficial TNF pathway activity.
As INmune continues exploring this innovative approach to combat cognitive decline related to TBI and AD, the results underscore the urgency of developing effective therapies for aging populations at risk. The data capture a critical translational link between inflammation and neurodegeneration, paving the way for further exploration in clinical settings.
MWN-AI** Analysis
**Market Analysis and Investment Advice on INmune Bio, Inc. (NASDAQ: INMB)**
INmune Bio, Inc. has recently garnered significant attention following promising data regarding its lead treatment candidate, XPro™ (XPro1595). This next-generation TNF inhibitor aims to target neuroinflammation, presenting a potential therapeutic avenue for conditions such as Alzheimer’s disease (AD), especially following traumatic brain injury (TBI). The recent presentation of data at the Keystone Symposia highlighted how XPro™ effectively reduces amyloid deposition and improves cognitive function in an AD animal model, signaling a step forward in AD research.
The current landscape for neurodegenerative treatment is dire, with increasing populations at risk as TBI is correlated with heightened Alzheimer's pathology. Given this backdrop, INmune Bio's strategic focus on TBI-related neuroinflammation positions it strongly within a significant and growing healthcare market. Analyzing XPro™'s potential, one sees not only the prospect of improving the quality of life for patients but also the corresponding market opportunity for investors.
However, potential investors should approach with caution. While initial findings are promising, clinical trials remain in the early stages, and FDA approval is uncertain. The biotechnology industry is fraught with risks, including the potential for trial delays or failures and dependency on further funding.
Investors should consider the volatility inherent in clinical-stage biotech companies and monitor the upcoming trial outcomes closely. Diversifying investments while keeping a particular focus on INmune Bio could mitigate risks associated with its development programs. Additionally, watch for partnerships or funding announcements, as collaboration with established institutions can bolster investor confidence.
In conclusion, while the potential of XPro™ and INmune Bio is considerable, prudent investors should maintain a balanced approach, weighing the promise of innovation against the realities of biotech investment risks.
**MWN-AI Summary and Analysis is based on asking OpenAI to summarize and analyze this news release.
XPro™ Treatment Post-TBI Prevents Short- and Long-Term Alzheimer’s-like Pathology in transgenic mice
Boca 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.
Traumatic 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.
The 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.
“Our 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.”
“Traumatic 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.”
Poster 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
About XPro™
XPro™ 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 .
About INmune Bio Inc.
INmune Bio Inc. is 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
Clinical 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.
Company Contact:
David Moss
Chief Financial Officer
(561) 710-0512
info@inmunebio.com
Daniel Carlson
Head of Investor Relations
(415) 509-4590
dcarlson@inmunebio.com
FAQ**
How does XPro™ Treatment from INmune Bio Inc. (NASDAQ: INMB) specifically target the solTNF/TNFR1 signaling pathway to reduce Alzheimer’s-like pathology post-TBI?
What are the potential implications of XPro™’s ability to mitigate BACE1 and A?42 levels in the context of Alzheimer’s disease prevention for INmune Bio Inc. (NASDAQ: INMB)?
Given the promising results of XPro™ in transgenic mice, what are the next steps for INmune Bio Inc. (NASDAQ: INMB) in advancing this treatment to human clinical trials?
How does INmune Bio Inc. (NASDAQ: INMB) plan to address the risks and uncertainties associated with the development of XPro™ and its potential market entry for Alzheimer's-related therapies?
**MWN-AI FAQ is based on asking OpenAI questions about INmune Bio Inc. (NASDAQ: INMB).
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