BOCA RATON, Fla., July 15, 2026
INmune Bio announced the publication of a peer-reviewed preclinical study in the Journal of Neurotrauma demonstrating that XPro1595, the company’s lead neuroinflammation candidate, prevented traumatic brain injury (TBI)-induced Alzheimer’s disease pathology, cognitive impairment, and pain in a preclinical model. The Department of Defense-funded study identified soluble tumor necrosis factor (sTNF) as a key biological link between traumatic brain injury and Alzheimer’s disease, suggesting that selective inhibition of sTNF may interrupt the inflammatory cascade that drives neurodegeneration.
XPro1595 Prevents Alzheimer’s-Related Brain Changes After Traumatic Brain Injury
The study found that a single moderate traumatic brain injury significantly increased brain levels of tumor necrosis factor (TNF), its receptor TNFR1, and the neurotoxic amyloid protein Aβ42, all of which are associated with Alzheimer’s disease progression. In contrast, treatment with XPro1595 prevented the injury-induced increase in amyloid pathology, reduced inflammatory signaling, improved learning and memory within one week of injury, and significantly reduced pain compared with untreated animals.
Soluble TNF Identified as a Key Driver of Neuroinflammation
Using the well-established 3xTg-AD mouse model of Alzheimer’s disease, researchers demonstrated that selectively neutralizing soluble TNF disrupted the inflammatory processes triggered by traumatic brain injury before amyloid accumulation could occur. The findings provide new evidence supporting soluble TNF as a critical mediator linking head injury to later Alzheimer’s disease and reinforce the role of neuroinflammation in disease development.
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Findings Support Continued Development of XPro1595 in Alzheimer’s Disease
INmune Bio noted that the results strengthen the scientific rationale behind XPro1595, a next-generation dominant-negative TNF therapy designed to selectively neutralize soluble TNF while preserving the protective immune functions mediated by transmembrane TNF. The company recently received FDA Fast Track Designation for XPro1595 and plans to advance the therapy into an integrated Phase 2b/3 seamless adaptive registrational program targeting neuroinflammation-enriched early Alzheimer’s disease. The new preclinical findings further support the potential of selective soluble TNF inhibition as a therapeutic strategy for Alzheimer’s disease and other neurodegenerative disorders associated with chronic neuroinflammation.
Source: INmune Bio press release
