INmune Bio’s XPro1595 Prevents Brain-Injury-Induced Alzheimer's Pathology, Memory Loss, and Pain in New Peer-Reviewed Preclinical Study
Rhea-AI Summary
INmune Bio (NASDAQ: INMB) reported new peer-reviewed preclinical data showing that selectively neutralizing soluble TNF with its lead candidate XPro1595 prevented traumatic-brain-injury–induced Alzheimer’s-type changes in a 3xTg-AD mouse model.
The Department of Defense–funded study, published in the Journal of Neurotrauma, found that a single moderate TBI increased brain levels of TNF, its receptor TNFR1, and the neurotoxic amyloid beta species Aβ42, and caused learning, memory, and pain-related deficits. Treatment with XPro1595 reduced TNF, blocked the injury-induced rise in Aβ42, improved learning and memory within one week of injury, and reduced pain compared with vehicle-treated injured animals. According to INmune Bio, the findings support soluble TNF as a key biological link between head injury and Alzheimer’s disease and reinforce soluble TNF neutralization as a potential neuroinflammation-targeted approach across neurodegenerative conditions.
Positive
- XPro1595 prevented TBI-induced rise in Aβ42 and improved cognition in 3xTg-AD mice
- Department of Defense–funded and published in peer-reviewed Journal of Neurotrauma
- XPro1595 reduced TNF, blocked amyloid pathology, and lowered pain versus vehicle after single TBI
Negative
- Evidence is from a preclinical 3xTg-AD mouse model, not human trials
- Study focuses on single moderate TBI, so broader injury scenarios are not addressed
News Market Reaction – INMB
In the Jul 15 session, INMB gained 2.48%, reflecting a moderate positive market reaction. Argus tracked a peak move of +2.4% during that session. Our momentum scanner triggered 5 alerts that day, indicating moderate trading interest and price volatility.
Data tracked by StockTitan Argus on the day of publication.
Historical Context
| Date | Event | Sentiment | 24h Move | Catalyst |
|---|---|---|---|---|
| Jul 09 | Phase 2 imaging data | Positive | +4.1% | Reported statistically significant Phase 2 imaging data for XPro in early Alzheimer’s. |
| Jul 01 | IP / patent update | Positive | +3.1% | Advanced CORDStrom MSC platform patent into U.S. national phase with long exclusivity potential. |
| Jun 25 | MHRA PIP approval | Positive | +10.4% | Received UK MHRA approval of Pediatric Investigation Plan for Ebstrocel in RDEB. |
| Jun 23 | Regulatory alignment | Positive | -0.7% | Obtained MHRA written alignment supporting planned 2026 UK conditional MAA for CORDStrom. |
| Jun 02 | Phase 2 biomarker data | Positive | +2.2% | Announced statistically significant white matter MRI biomarker effects in MINDFuL Alzheimer’s trial. |
24h Move is the share-price change in the day after each event; other market factors may also have contributed.
Recent INmune Bio news, especially around XPro and CORDStrom, has more often coincided with positive price reactions than with selloffs.
Key Terms
soluble TNF medical
amyloid beta medical
Aβ42 medical
traumatic brain injury medical
neuroinflammation medical
AI-generated analysis. How Rhea-AI works. Not financial advice.
The study points to soluble TNF as a key biological link between head injury and Alzheimer’s disease and shows that selectively neutralizing it with XPro1595 prevents the injury-induced rise in amyloid pathology while improving early cognitive and pain-related outcomes.
Boca Raton, FL, July 15, 2026 (GLOBE NEWSWIRE) -- INmune Bio, Inc. (NASDAQ: INMB), a late-stage inflammation and immunology company, today announced the publication of a new peer-reviewed preclinical study in the Journal of Neurotrauma examining how traumatic brain injury (TBI) drives the biological changes that link head injury to Alzheimer’s disease (AD). The Department of Defense–funded study; entitled: “Inhibition of Soluble TNF Mitigates Traumatic Brain Injury as a Risk Factor for the Development of Amyloidogenic Proteins and Functional Deficits in 3xTg-AD Mice”; found that a single brain injury raised two proteins central to Alzheimer’s biology, the inflammatory cytokine tumor necrosis factor (TNF) and the neurotoxic form of amyloid beta (Aβ42), and that treatment with the Company’s lead neuroinflammation candidate, XPro1595, prevented the injury-induced rise in amyloid pathology.
TBI is among the strongest environmental risk factors for later dementia, yet the biology linking the two has been unclear. These findings implicate soluble TNF, the disease-driving form of the cytokine, as a key link, and show that selectively neutralizing it can interrupt the inflammatory cascade before amyloid pathology takes hold.
TBI raised brain levels of TNF, its receptor TNFR1, and Aβ42, and produced deficits in learning and memory and pain. In comparison, animals treated with XPro1595 showed reduced TNF, no injury-induced rise in Aβ42, improved learning and memory within one week of injury, and reduced pain compared to vehicle-treated injured animals.
“For a long time we’ve known that a traumatic brain injury raises the risk of Alzheimer’s disease without really understanding why. These data point to soluble TNF as a key part of that link: neutralizing it early kept the injury from triggering the rise in amyloid-related proteins and prevented the memory and pain deficits that usually follow, reinforcing how central neuroinflammation is to the onset of Alzheimer’s pathology,” said study author (and funding Principal Investigator) Dr. Kirsty Dixon, Associate Professor of Surgery at Virginia Commonwealth University. “While we’ll continue to study the relationship between inflammation and Alzheimer’s, these findings suggest there may be a role in the treatment continuum for selectively targeting soluble TNF, both for younger people who suffer a head injury and for Alzheimer’s patients, who are especially prone to falls and other injuries.”
Male 3xTg-AD mice, a well-characterized Alzheimer’s model, received either a single moderate TBI or a sham procedure and were treated with either XPro1595 or vehicle. Researchers measured brain cytokines, inflammatory markers, and AD-related proteins such as Aβ42, and assessed the animals for deficits in cognition and mechanical hypersensitivity.
“These independent findings reinforce the thesis behind our approach: selectively neutralizing soluble TNF to interrupt the neuroinflammation that drives Alzheimer’s pathology. Seeing that mechanism prevent both amyloid accumulation and functional decline in a model of injury-accelerated Alzheimer’s adds to a growing body of evidence supporting soluble TNF as a target across neurodegenerative disease,” said David Moss, Chief Executive Officer of INmune Bio.
About XPro™
XPro1595 is a next-generation inflammatory cytokine modulator that neutralizes soluble TNF (sTNF) without affecting transmembrane TNF (tmTNF) or its receptors. This selective targeting is designed to reduce neuroinflammation, a key driver of neurodegeneration in Alzheimer’s disease, while maintaining the protective immune functions of the body.
About INmune Bio Inc.
INmune Bio Inc. is a publicly traded (NASDAQ: INMB), late-stage biotechnology company focused on developing treatments that target the innate immune system to fight disease. Moving beyond early-stage exploration, the company’s clinical-development strategy centers on advanced precision medicine, matching drug mechanisms directly to patient biology to optimize clinical outcomes.
INmune Bio is actively advancing two late-stage product platforms toward registrational milestones:
- CORDStrom™: A proprietary, pooled, allogeneic, human umbilical cord-derived mesenchymal stromal cell (hucMSC) platform engineered to address the historical clinical challenges of donor variability and manufacturing inconsistency. Following successful clinical readouts in Recessive Dystrophic Epidermolysis Bullosa (RDEB), the platform is transitioning to regulatory filing phases, with a Marketing Authorization Application (MAA) scheduled for the UK MHRA and EU EMA in 2026, alongside a planned U.S. Biologics License Application (BLA) submission.
- XPro™ (XPro1595): A Dominant-Negative Tumor Necrosis Factor (DN-TNF) platform that selectively neutralizes soluble TNF (sTNF) to eliminate neuroinflammation without compromising protective immune function. Backed by recently granted FDA Fast Track designation and successful regulatory alignment from an End-of-Phase 2 meeting, XPro™ is positioned for an integrated Phase 2b/3 seamless adaptive registrational program in neuroinflammation-enriched early Alzheimer's disease.
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 related to the development or commercialization of product candidates and other business and financial matters, including without limitation, trial results and data, including trial results, timing of key milestones, future plans or expectations, and the prospects for receiving regulatory approval or commercializing or selling any product or drug candidates, 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®™ have either finished clinical trials, are still in clinical trials or are preparing to start clinical trials and have not been approved by the US Food and Drug Administration (FDA), the UK MHRA or any regulatory body and there cannot be any assurance that they will be approved by the FDA, the UK MHRA 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.
INmune Bio Contacts:
David Moss
Chief Executive Officer
(561) 710-0512
info@inmunebio.com
Daniel Carlson
Head of Investor Relations
(415) 509-4590
dcarlson@inmunebio.com
