INMB News & Events

INmune Bio announced that results from its Phase 2 MINDFuL trial in Alzheimer's disease have been published in the peer-reviewed journal NPJ Dementia. The study evaluated the safety, biomarker engagement, and clinical efficacy of XPro in patients with mild Alzheimer's disease characterized by biomarkers of inflammation. In a pre-specified analysis of the protocol-defined Alzheimer's Disease with inflammation subgroup, XPro showed directionally consistent benefit across cognitive, global, functional, behavioral, and biomarker endpoints over 24 weeks, with no amyloid-related imaging abnormalities observed. The publication discusses how XPro demonstrated consistent positive trends in a pre-specified enriched subpopulation with amyloid-beta positivity and two or more inflammation biomarkers. The paper further highlights the effect sizes up to 0.27 across cognitive, Patient-Reported Outcomes, behavioral and biomarker endpoints, directionally consistent with an XPro treatment effect. These findings support prioritization of the enriched population in future studies to optimize detection of treatment effects.

INmune Bio announced that the FDA has granted fast track designation to XPro, the company's selective soluble TNF inhibitor, for the treatment of early Alzheimer's disease. The designation specifically covers XPro for treatment of early Alzheimer's disease encompassing both mild cognitive impairment due to AD and mild Alzheimer's disease dementia.

INmune Bio announces new preclinical data for INB03. The data will be presented at the American Association for Cancer Research, AACR, Annual Meeting 2026 in San Diego on April 17-22. Key Scientific Findings: Overcoming Resistance in Vitro: The combination of INB03 with either lapatinib or tucatinib produced statistically superior inhibition of cell proliferation and migration in both HER2+ JIMT-1 and brain-metastatic JIMT-1 Br3-luc cell lines compared to TKIs alone. Enhanced Tumor Control In Vivo: In female nude mice bearing JIMT-1 or JIMT-1 Br3-luc tumors, INB03 + TKI combinations markedly slowed tumor growth compared to TKIs alone. Reduction of Metastatic Spread: The addition of INB03 significantly reduced the incidence of metastases to brain, lung, and liver. Notably, it further enhanced tucatinib's effect on lung metastases. Mechanism of Action: These results support prior research showing that selective sTNF neutralization with INB03 down-regulates MUC4, a protein that shields the HER2 molecule and prevents therapies from binding effectively.