{"id":981649,"date":"2026-07-15T07:06:39","date_gmt":"2026-07-15T11:06:39","guid":{"rendered":"https:\/\/www.marketnewsdesk.com\/index.php\/inmune-bios-xpro1595-prevents-brain-injury-induced-alzheimers-pathology-memory-loss-and-pain-in-new-peer-reviewed-preclinical-study\/"},"modified":"2026-07-15T07:06:39","modified_gmt":"2026-07-15T11:06:39","slug":"inmune-bios-xpro1595-prevents-brain-injury-induced-alzheimers-pathology-memory-loss-and-pain-in-new-peer-reviewed-preclinical-study","status":"publish","type":"post","link":"https:\/\/www.marketnewsdesk.com\/index.php\/inmune-bios-xpro1595-prevents-brain-injury-induced-alzheimers-pathology-memory-loss-and-pain-in-new-peer-reviewed-preclinical-study\/","title":{"rendered":"INmune Bio\u2019s XPro1595 Prevents Brain-Injury-Induced Alzheimer’s Pathology, Memory Loss, and Pain in New Peer-Reviewed Preclinical Study"},"content":{"rendered":"
\n

\n The study points to soluble TNF as a key biological link between head injury and Alzheimer\u2019s 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.<\/i>\n <\/p>\n

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\u2019s disease (AD). The Department of Defense\u2013funded study; entitled: \u201cInhibition of Soluble TNF Mitigates Traumatic Brain Injury as a Risk Factor for the Development of Amyloidogenic Proteins and Functional Deficits in 3xTg-AD Mice\u201d; found that a single brain injury raised two proteins central to Alzheimer\u2019s biology, the inflammatory cytokine tumor necrosis factor (TNF) and the neurotoxic form of amyloid beta (A\u03b242), and that treatment with the Company\u2019s lead neuroinflammation candidate, XPro1595, prevented the injury-induced rise in amyloid pathology.<\/p>\n

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.<\/p>\n

TBI raised brain levels of TNF, its receptor TNFR1, and A\u03b242, and produced deficits in learning and memory and pain. In comparison, animals treated with XPro1595 showed reduced TNF, no injury-induced rise in A\u03b242, improved learning and memory within one week of injury, and reduced pain compared to vehicle-treated injured animals.<\/p>\n

\u201cFor a long time we\u2019ve known that a traumatic brain injury raises the risk of Alzheimer\u2019s 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\u2019s pathology,\u201d said study author (and funding Principal Investigator) Dr. Kirsty Dixon, Associate Professor of Surgery at Virginia Commonwealth University.\u00a0 \u201cWhile we\u2019ll continue to study the relationship between inflammation and Alzheimer\u2019s, 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\u2019s patients, who are especially prone to falls and other injuries.\u201d<\/p>\n

Male 3xTg-AD mice, a well-characterized Alzheimer\u2019s 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 A\u03b242, and assessed the animals for deficits in cognition and mechanical hypersensitivity.<\/p>\n

\u201cThese independent findings reinforce the thesis behind our approach: selectively neutralizing soluble TNF to interrupt the neuroinflammation that drives Alzheimer\u2019s pathology. Seeing that mechanism prevent both amyloid accumulation and functional decline in a model of injury-accelerated Alzheimer\u2019s adds to a growing body of evidence supporting soluble TNF as a target across neurodegenerative disease,\u201d said David Moss, Chief Executive Officer of INmune Bio.<\/p>\n

\n About XPro\u2122<\/b>\n <\/p>\n

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\u2019s disease, while maintaining the protective immune functions of the body.<\/p>\n

\n About INmune Bio Inc.<\/b>\n <\/p>\n

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\u2019s clinical-development strategy centers on advanced precision medicine, matching drug mechanisms directly to patient biology to optimize clinical outcomes.<\/p>\n

INmune Bio is actively advancing two late-stage product platforms toward registrational milestones:<\/p>\n

    \n
  1. \n CORDStrom\u2122:<\/b> 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.<\/li>\n
  2. \n XPro\u2122 (XPro1595):<\/b> 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\u2122 is positioned for an integrated Phase 2b\/3 seamless adaptive registrational program in neuroinflammation-enriched early Alzheimer’s disease.<\/li>\n<\/ol>\n

    \n Forward Looking Statements<\/b>\n <\/p>\n

    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\u2122, XPro1595\u2122 (XPro\u2122, pegipanermin), and INKmune\u00ae\u2122 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\u2019s 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\u2019s 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\u2019s filings with the Securities and Exchange Commission, including the Company\u2019s Annual Report on Form 10-K, the Company\u2019s Quarterly Reports on Form 10-Q and the Company\u2019s 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.<\/p>\n

    \n INmune Bio\u00a0Contacts:<\/b>
    \n
    David Moss
    Chief Executive Officer
    (561) 710-0512
    info@inmunebio.com<\/a>
    <\/a>
    <\/a>Daniel Carlson
    Head of Investor Relations
    (415) 509-4590
    dcarlson@inmunebio.com<\/a><\/p>\n

    \"\"
    \n
    \n \"\"\n <\/div>\n

    <\/div>\n","protected":false},"excerpt":{"rendered":"

    The study points to soluble TNF as a key biological link between head injury and Alzheimer\u2019s 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\u2019s disease (AD). The Department of Defense\u2013funded study; entitled: \u201cInhibition of Soluble TNF Mitigates Traumatic Brain Injury as a Risk Factor for the Development of Amyloidogenic Proteins and Functional Deficits in … <\/p>\n

    Continue reading “INmune Bio\u2019s XPro1595 Prevents Brain-Injury-Induced Alzheimer’s Pathology, Memory Loss, and Pain in New Peer-Reviewed Preclinical Study”<\/span><\/a><\/p>\n","protected":false},"author":2,"featured_media":0,"comment_status":"closed","ping_status":"closed","sticky":false,"template":"","format":"standard","meta":{"footnotes":""},"categories":[],"tags":[],"class_list":["post-981649","post","type-post","status-publish","format-standard","hentry"],"yoast_head":"\nINmune Bio\u2019s XPro1595 Prevents Brain-Injury-Induced Alzheimer's Pathology, Memory Loss, and Pain in New Peer-Reviewed Preclinical Study - Market Newsdesk<\/title>\n<meta name=\"robots\" content=\"index, follow, max-snippet:-1, max-image-preview:large, max-video-preview:-1\" \/>\n<link rel=\"canonical\" href=\"https:\/\/www.marketnewsdesk.com\/index.php\/inmune-bios-xpro1595-prevents-brain-injury-induced-alzheimers-pathology-memory-loss-and-pain-in-new-peer-reviewed-preclinical-study\/\" \/>\n<meta property=\"og:locale\" content=\"en_US\" \/>\n<meta property=\"og:type\" content=\"article\" \/>\n<meta property=\"og:title\" content=\"INmune Bio\u2019s XPro1595 Prevents Brain-Injury-Induced Alzheimer's Pathology, Memory Loss, and Pain in New Peer-Reviewed Preclinical Study - Market Newsdesk\" \/>\n<meta property=\"og:description\" content=\"The study points to soluble TNF as a key biological link between head injury and Alzheimer\u2019s 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. 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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\u2019s disease (AD). The Department of Defense\u2013funded study; entitled: \u201cInhibition of Soluble TNF Mitigates Traumatic Brain Injury as a Risk Factor for the Development of Amyloidogenic Proteins and Functional Deficits in … Continue reading \"INmune Bio\u2019s XPro1595 Prevents Brain-Injury-Induced Alzheimer’s Pathology, Memory Loss, and Pain in New Peer-Reviewed Preclinical Study\"","og_url":"https:\/\/www.marketnewsdesk.com\/index.php\/inmune-bios-xpro1595-prevents-brain-injury-induced-alzheimers-pathology-memory-loss-and-pain-in-new-peer-reviewed-preclinical-study\/","og_site_name":"Market Newsdesk","article_published_time":"2026-07-15T11:06:39+00:00","og_image":[{"url":"https:\/\/www.globenewswire.com\/newsroom\/ti?nf=OTc2MjQwMCM3NzA2ODM4IzUwMDA2ODMyNA==","type":"","width":"","height":""}],"author":"Newsdesk","twitter_card":"summary_large_image","twitter_misc":{"Written by":"Newsdesk","Est. reading time":"6 minutes"},"schema":{"@context":"https:\/\/schema.org","@graph":[{"@type":"Article","@id":"https:\/\/www.marketnewsdesk.com\/index.php\/inmune-bios-xpro1595-prevents-brain-injury-induced-alzheimers-pathology-memory-loss-and-pain-in-new-peer-reviewed-preclinical-study\/#article","isPartOf":{"@id":"https:\/\/www.marketnewsdesk.com\/index.php\/inmune-bios-xpro1595-prevents-brain-injury-induced-alzheimers-pathology-memory-loss-and-pain-in-new-peer-reviewed-preclinical-study\/"},"author":{"name":"Newsdesk","@id":"https:\/\/www.marketnewsdesk.com\/#\/schema\/person\/482f27a394d4fda80ecb5499e519d979"},"headline":"INmune Bio\u2019s XPro1595 Prevents Brain-Injury-Induced Alzheimer’s Pathology, Memory Loss, and Pain in New Peer-Reviewed Preclinical Study","datePublished":"2026-07-15T11:06:39+00:00","mainEntityOfPage":{"@id":"https:\/\/www.marketnewsdesk.com\/index.php\/inmune-bios-xpro1595-prevents-brain-injury-induced-alzheimers-pathology-memory-loss-and-pain-in-new-peer-reviewed-preclinical-study\/"},"wordCount":1163,"image":{"@id":"https:\/\/www.marketnewsdesk.com\/index.php\/inmune-bios-xpro1595-prevents-brain-injury-induced-alzheimers-pathology-memory-loss-and-pain-in-new-peer-reviewed-preclinical-study\/#primaryimage"},"thumbnailUrl":"https:\/\/www.globenewswire.com\/newsroom\/ti?nf=OTc2MjQwMCM3NzA2ODM4IzUwMDA2ODMyNA==","inLanguage":"en-US"},{"@type":"WebPage","@id":"https:\/\/www.marketnewsdesk.com\/index.php\/inmune-bios-xpro1595-prevents-brain-injury-induced-alzheimers-pathology-memory-loss-and-pain-in-new-peer-reviewed-preclinical-study\/","url":"https:\/\/www.marketnewsdesk.com\/index.php\/inmune-bios-xpro1595-prevents-brain-injury-induced-alzheimers-pathology-memory-loss-and-pain-in-new-peer-reviewed-preclinical-study\/","name":"INmune Bio\u2019s XPro1595 Prevents Brain-Injury-Induced Alzheimer's Pathology, Memory Loss, and Pain in New Peer-Reviewed Preclinical Study - 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