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Drug Development.

Rishi K Somvanshi1, Shadi Madani2, Sneha Singh2

  • 1North Island College, Courtenay, BC, Canada.

Alzheimer'S & Dementia : the Journal of the Alzheimer'S Association
|December 26, 2025
PubMed
Summary
This summary is machine-generated.

A novel synthetic cannabinoid, INM-901, reversed Alzheimer

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Area of Science:

  • Neuroscience
  • Pharmacology
  • Genetics

Background:

  • Alzheimer's Disease (AD) is a progressive neurodegenerative disorder impacting millions, with current treatments offering only symptomatic relief.
  • Existing therapies, including amyloid beta (Aβ) antibody treatments, face limitations in efficacy and tolerability.
  • Cannabinoids show promise in mitigating AD pathology by targeting Aβ toxicity, tau phosphorylation, and neuroinflammation.

Purpose of the Study:

  • To investigate the therapeutic potential of a novel synthetic cannabinoid analogue, INM-901, in an Alzheimer's Disease mouse model.
  • To evaluate the effects of INM-901 on Aβ-induced toxicity, neuroinflammation, and cognitive/sensorimotor deficits.

Main Methods:

  • Male 5xFAD mice, exhibiting AD-like pathology, were administered INM-901 (15 or 30 mg/kg) or vehicle twice-weekly for 7 months.
  • Behavioral assessments included Open-field, Zero Maze, Barnes Maze, and Acoustic Startle Response tests.
  • Molecular analyses involved RNAseq, immunohistochemistry, western blotting, and multiplex assays to assess AD-related markers.

Main Results:

  • INM-901 treatment significantly improved cognitive functions, spatial learning, and memory in the Barnes Maze.
  • The compound reversed anxiety-like behaviors and enhanced auditory processing as indicated by acoustic startle response.
  • INM-901 reduced expression of inflammatory genes, pro-inflammatory cytokines, neurofilament light chain (NfL), and Aβ-aggregation, while modulating CB2R expression.

Conclusions:

  • INM-901 demonstrated significant neuroprotective and anti-inflammatory effects in a mouse model of Alzheimer's Disease.
  • The study highlights INM-901's potential as a therapeutic candidate for AD, warranting further investigation in other neurodegenerative models.