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InMed's INM-901 Demonstrates Statistically Significant Reduction in Neuroinflammation in a Long-Term Preclinical Alzheimer's Disease Study
INM-901 significantly reduced pro-inflammatory cytokines associated with Alzheimer's Statistically significant reduction in neurodegeneration marker,
About this update from Inmed Pharmaceuticals Inc.
[{"type":"text","content":"\n\nINM-901 significantly reduced pro-inflammatory cytokines associated with Alzheimer's\n\n\nStatistically significant reduction in neurodegeneration marker, neurofilament light chain ('NfL')\n\n\nmRNA profile showed a reduction of several key neuroinflammatory genes in the brain\n\n\nVancouver, British Columbia--(Newsfile Corp. - January 21, 2025) - InMed Pharmaceuticals Inc. (NASDAQ: INM) (\"InMed\" or the \"Company\"), a pharmaceutical company focused on developing a pipeline of proprietary small molecule drug candidates for diseases with high unmet medical needs, today announces positive results from a long-term in vivo preclinical Alzheimer's Disease ('AD') study. In the study, INM-901 demonstrated a reduction in several plasma and brain markers of neuroinflammation, a recognized contributor to Alzheimer's disease development and progression.\nResults from the long-term study of INM-901 in a well-characterized Alzheimer's disease model demonstrated the following:\n\n\nImproved cytokine profile - INM-901 treated groups showed a dose-dependent and statistically significant reduction in plasma pro-inflammatory cytokines such as TNF-α, IL-1ß and INF-γ. Cytokine networks, when deregulated, may contribute to tissue inflammation.\n\n\nReduction in neurodegeneration biomarker - INM-901 demonstrated a dose-dependent and statistically significant reduction in neurofilament light chain ('NfL') in the plasma for the high dose treated group. NfL is a protein that is released from neurons in response to injury or disease. NfL levels are used to assess cellular damage in neurodegenerative disease.\n\n\nStudy supported by mRNA data - mRNA assessments showed a reduction of several key neuroinflammatory genes in the brain, such as GFAP, CD-33 and TLR-2, further supporting the overall results from the study.\n\n\nDr. Eric Hsu, InMed's SVP of Preclinical R&D, commented, \"We are highly encouraged by the data from our long-term preclinical study of INM-901. Overall, our data showed a reduction of several neuroinflammation markers in an amyloid-induced Alzheimer's disease model, suggesting that INM-901 may lower neuroinflammation. The ability of INM-901 to actively reduce inflammation is an exciting development, as neuroinflammation has emerged as a promising new drug target beyond existing AD treatments focused primarily on removing amyloid be...