InMed Pharmaceuticals Inc. (NASDAQ: INM) announced new preclinical data demonstrating that its proprietary small molecule drug candidate INM-901 significantly reduces neuroinflammation in ex vivo models, further supporting its therapeutic potential in Alzheimer's disease. The Vancouver-based pharmaceutical company reported that the compound achieved statistically significant reductions in multiple pro-inflammatory markers associated with neurodegeneration.
Study Design and Key Findings
The study evaluated INM-901 using an ex vivo model of lipopolysaccharide (LPS)-induced inflammation in animal brain tissue. This model was designed to induce strong expression of pro-inflammatory cytokines IL-6, IL-1β, IL-2, and KC/Gro, along with the inflammasome marker NLRP3.
Results demonstrated that INM-901 treatment produced dose-dependent and statistically significant reductions in several key pro-inflammatory markers. Most notably, the compound significantly reduced levels of NLRP3 and IL-1β, two inflammasome markers increasingly implicated in the pathogenesis of Alzheimer's disease and other neuroinflammatory diseases.
Independent Anti-Inflammatory Mechanism
A particularly significant finding was that INM-901 reduced key pro-inflammatory markers independent of amyloid beta or tau pathology. This suggests the compound may have direct effects on neuroinflammation that could extend beyond traditional Alzheimer's disease mechanisms, potentially offering therapeutic benefits for other dementia-related diseases.
"NLRP3-driven inflammation is recognized as a key contributor to neurodegenerative disease progression," said Dr. Eric Hsu, SVP of Preclinical Research & Development at InMed. "The data derived from this LPS-induced inflammation study further support our previous findings in the amyloid beta animal model following INM-901 treatment, which demonstrated a significant reduction in inflammatory markers."
Clinical Significance of NLRP3 Targeting
NLRP3 has been implicated in the pathogenesis of several inflammatory, autoimmune, metabolic and neurodegenerative conditions including Alzheimer's disease, Parkinson's disease, and type 2 diabetes. In these diseases, overactivation of NLRP3 can result in chronic brain inflammation, which may contribute to neurodegeneration and cognitive decline.
INM-901 Program Overview
INM-901 is characterized as a proprietary small molecule drug candidate with potentially multiple mechanisms of action for Alzheimer's disease. The compound functions as a preferential signaling agonist of CB1/CB2 receptors and has demonstrated neuroprotective effects in preclinical studies.
Key characteristics of INM-901 include its ability to reduce neuroinflammation and improve neurite growth and neuronal function, indicating potential to restore damage caused by Alzheimer's disease. The compound also impacts peroxisome proliferator-activated receptors (PPARs), which play important roles in diabetes and are considered potential therapeutic targets for neurodegenerative disorders.
From an administration perspective, INM-901 can be delivered orally and achieve therapeutic levels in the brain comparable to those obtained through intraperitoneal injection. In long-term preclinical behavioral studies, the compound has demonstrated significant improvements in cognitive function, memory, locomotor activity, anxiety-based behavior, and sound awareness.
Development Timeline
InMed plans to advance INM-901 through additional preclinical studies, with IND-enabling studies to follow. The company positions this latest study as a key advancement for the program, highlighting INM-901 as a distinctive and promising therapeutic candidate for Alzheimer's disease treatment.
