Pre-Clinical Studies

Efficacy of rhu-pGSN replacement has been demonstrated in 18 animal models conducted by many independent laboratories.

Replenishment of deficient pGSN levels has been shown to have significant medical relevance because it:

  • Prevents inflammatory dysregulation and progression to systemic inflammation in a myriad of chronic and acute diseases
  • Boosts the immune response to increase survival in infectious disease

This provides a strong rationale for clinical effectiveness in both inflammatory and infectious disease conditions.

Efficacy of rhu-pGSN replacement has been demonstrated in 18 animal models conducted by many independent laboratories. These include:

    Infection (bacterial, viral):

  • Gram Positive-S. pneumoniae (mice)
  • Influenza with S. pneumoniae super-infection (mice)
  • Infectious Peritonitis Model (mice)
  • Influenza (mice)
  • Infectious Peritonitis Model (rat)
  • Endotoxin/LPS Challenge (mice)

     Injury/Trauma:

  • Burn Injury of Lung Microvascular Permeability (rat)
  • Hyperoxia Acute Lung Injury (mice)
  • Neuroinflammation (mice)
  • Radiation Exposure Model (mice)

     Inflammation/CV/Metabolic:

  • Ischemic Stroke Model (rat)
  • Inflammatory Bowel Disease (rats)
  • Diabetes Type 2: HFD/STZ C57 and db/db models (mice)
  • Pain: Carrageenan-induced paw edema, acetic acid writing, tail immersion (mice)

     Neurological:

  • Alzheimer’s Disease Reduction in Plaque (mice)
  • Multiple Sclerosis model (mice)