InMed Pharmaceuticals Inc. (NASDAQ:INM) ("InMed" or the "Company"), a pharmaceutical company developing a pipeline of disease-modifying small molecule drug candidates targeting CB1 and CB2 receptors, today announced new preclinical data demonstrating the effects of INM-901 in reducing neuroinflammation in 3D human brain organoid models of Alzheimer's disease.

These studies, conducted in collaboration with Stem Pharm, Inc. ("Stem Pharm") using their proprietary platform of human neuro-immune organoids, represent a key step in translating prior animal model results for INM-901 into a human-relevant system, helping to de-risk the INM-901 program ahead of a first-in-human clinical trial.

The in vitro human organoid models represent some of the closest approximations to human brain tissue currently available, incorporating a complex cellular environment relevant to neurodegenerative disease. The organoids are composed of neurons, astrocytes, vascular cells and feature microglia, the brain's resident immune cells, and can be used to bridge the gap between traditional animal models and human clinical trials.

INM-901 was evaluated in two distinct human 3D organoid models: a general model of neuroinflammation induced with lipopolysaccharide ("LPS") and interferon-gamma ("IFN-γ"); and, Stem Pharm's proprietary neuroinflammation Alzheimer's disease model with specific features observed in Alzheimer's disease patients.

Key Observations:

  • INM-901 demonstrated significant reduction in neuroinflammation in Stem Pharm's LPS-induced model and in their Alzheimer's disease model. A dose-dependent reduction of key pro-inflammatory markers such as IL-6 and IL-8 was seen in both neuroinflammation models.
  • Effects align with prior findings from an in vivo Alzheimer's model and an ex vivo LPS-induced neuroinflammation model.
  • Provides supportive evidence of mechanistic translation from animal models to human tissue systems.

The consistency of INM-901's anti-inflammatory effects across in vivo animal models, ex vivo systems and now human 3D brain organoids provide increasing confidence in the compound's potential to translate into clinical benefit in humans with neuroinflammatory conditions.

Dr. Eric Hsu, InMed SVP of Preclinical Research and Development, commented, "These results represent an important milestone for INM-901. We have now demonstrated consistent anti-neuroinflammatory effects across multiple in vivo and ex vivo studies, and, importantly, these findings have now been translated into advanced human brain organoid systems. This systematic validation significantly de-risks the program and strengthens our confidence as we advance INM-901 toward human clinical trials."

Key Datasets impacting Anti-Neuroinflammation to date:

• In a long-term mouse model mimicking Alzheimer's disease, INM-901 significantly reduced inflammatory biomarkers IFN-γ, TNF-α, IL-1β, KC-GRO, IL-2 and neurodegenerative marker neurofilament light chain ("NfL").

• INM-901 significantly reduced inflammasome activation and multiple pro-inflammatory cytokines, including NLRP3, IL-1β, IL-6, IL-2 and KC-GRO in an LPS-induced neuroinflammation ex vivo model, demonstrated anti-inflammatory effects independent of amyloid-beta or tau pathology.

• Reduction of neuroinflammation in 3D human brain organoid models of Alzheimer's disease.

Next Steps for the INM-901 Program for Alzheimer's Disease

• Conduct a pre-IND meeting with the U.S. Food and Drug Administration in Q3/2026.

• Continue to execute on IND-enabling pharmacology and toxicology studies.

• Continued development and scale-up of drug substance and product manufacturing activities to support IND enabling studies and submission.

• Engage regulatory/clinical experts in neurodegenerative diseases to map out topline clinical design for first-in-human clinical trials for the INM-901.

• Subject to regulatory feedback and completion of IND-enabling activities, the Company targets submission of an IND and initiation of a Phase 1 clinical trial in 2027.