ImSAIDs®

Immune Selective Anti-Inflammatory Derivatives – Imagine being able to target inflammation at its source!

Background: Leukocyte (white blood cell) activation and transmigration are the earliest and most important events that occur during inflammation.  Leukocytes, which participate in all inflammatory processes, are necessary in host defense but excessive and inappropriate activation can result in worsening of pathology.  Granulocytes, in particular, release a spectrum of substances which amplify the inflammatory cascade as illustrated in pancreatitis, sepsis, asthma, ischemic reperfusion injury, trauma, hepatitis, etc.

Conventional non-steroidal drugs (COX inhibiting NSAIDs) and glucocorticoids are not designed to specifically modulate leukocyte trafficking and are contraindicated in a variety of diseases and inflammatory events.  In summary, the current anti-inflammatory repository is deficient for a variety of inflammatory and critical care indications which propose to be satisfied by the ImSAIDs.

ImSAIDs Description: ImSAIDs are amino acid complexes that help support anti-inflammatory activity by aiding in the reduction of over-activation of leukocytes.  Previous studies have shown the ImSAIDs to exert their effects by supporting immune health by supporting granulocyte activity1,2,3,4, , reducing the production of reactive oxygen species5, reducing the effects of endotoxin6,7, and reducing allergic and anaphylactic reactions8,9,10

REFERENCES

  1. Bao F, John SM, Chen Y, Mathison RD, Weaver LC. The tripeptide phenylalanine-(D) glutamate-(D) glycine modulates leukocyte infiltration and oxidative damage in rat injured spinal cord. Neuroscience. 2006 Jul 7;140(3):1011-22. Epub 2006 Apr 3.
  2. Mathison RD, Befus AD, Davison JS, Woodman RC. Modulation of neutrophil function by the tripeptide feG. BMC Immunol. 2003 Mar 4;4:3. Epub 2003 Mar 4.
  3. Mathison R, Woodman R, Davison JS. Regulation of leukocyte adhesion to heart by the tripeptides feG and feG(NH2). Can J Physiol Pharmacol. 2001 Sep;79(9):785-92.
  4. Dery RE, Ulanova M, Puttagunta L, Stenton GR, James D, Merani S, Mathison R, Davison J, Befus AD. Frontline: Inhibition of allergen-induced pulmonary inflammation by the tripeptide feG: a mimetic of a neuro-endocrine pathway. Eur J Immunol. 2004 Dec;34(12):3315-25.
  5. Mathison RD, Davison JS. The Tripeptide feG Regulates the Production of Intracellular Reactive Oxygen Species by Neutrophils. J Inflamm (Lond). 2006 Jun 15;3(1):9
  6. Mathison R, Lo P, Tan D, Scott B, Davison JS. The tripeptide feG reduces endotoxin-provoked perturbation of intestinal motility and inflammation. Neurogastroenterol Motil. 2001 Dec;13(6):599-603.
  7. Tan D, Rougeot C, Davison JS, Mathison R. The carboxamide feG(NH2) inhibits endotoxin perturbation of intestinal motility. Eur J Pharmacol. 2000 Dec 8;409(2):203-5.
  8. Mathison R, Lo P, Moore G, Scott B, Davison JS. Attenuation of intestinal and cardiovascular anaphylaxis by the salivary gland tripeptide FEG and its D-isomeric analog feG. Peptides. 1998;19(6):1037-42.
  9. Dery RE, Mathison R, Davison J, Befus AD. Inhibition of allergic inflammation by C-terminal peptides of the prohormone submandibular rat 1 (SMR-1). Int Arch Allergy Immunol. 2001 an-Mar;124(1-3):201-4.
  10. Mathison RD, Davison JS, Befus AD. The tripeptide feG reduces perturbation of intestinal motility provoked by anaphylaxis. Proc West Pharmacol Soc. 2001;44:157-8.