Therapeutic Approach for Autoimmune Diseases, Inflammatory Diseases and Cancers by Blocking CIKS-TRAF6 Interactions
Posted Mar 14 2011 8:00pm
Description of Invention: CIKS (also known as Act1 or TRAF3IP2) is an intracellular adaptor protein involved in the signaling pathway of IL-17 cytokines. Interaction between CIKS and tumor necrosis factor receptor-associated factor (TRAF 6) is important for IL-17 signaling and collectively, IL-17, CIKS, and TRAF6 are involved in inflammatory responses associated with autoimmune diseases, inflammatory diseases, and cancers. Inhibition of CIKS activity has been shown to prevent and alleviate pathological symptoms in an animal model of rheumatoid arthritis and multiple sclerosis, and it is hypothesized that disruption of the interaction between CIKS and TRAF6 is a therapeutic strategy for the selective prevention of certain IL-17-mediated diseases.
NIAID investigators have discovered a short sequence within CIKS that is responsible for CIKS interaction with TRAF6. The disclosed sequence can be used to develop blocking peptides for the treatment of IL-17-mediated autoimmune diseases, inflammatory diseases, and cancers.
Applications: Therapeutics for IL-17-mediated diseases, such as inflammatory diseases, autoimmune diseases, and cancer
Advantages: Selective inhibition of CIKS-TRAF6 interactions
Development Status: Basic research
Inventors: Ulrich Siebenlist (NIAID) Soeren U Soender (NIAID) Sun Saret (NIAID)
Portfolios: Cancer Cancer - Therapeutics Internal Medicine Internal Medicine - Therapeutics
For Licensing Information Please Contact: Tara Kirby Ph.D. NIH Office of Technology Transfer 6011 Executive Blvd. Suite 325, Rockville, MD 20852 United States Email: tk200h@nih.gov Phone: 301-435-4426 Fax: 301-402-0220
Description of Invention:
CIKS (also known as Act1 or TRAF3IP2) is an intracellular adaptor protein involved in the signaling pathway of IL-17 cytokines. Interaction between CIKS and tumor necrosis factor receptor-associated factor (TRAF 6) is important for IL-17 signaling and collectively, IL-17, CIKS, and TRAF6 are involved in inflammatory responses associated with autoimmune diseases, inflammatory diseases, and cancers. Inhibition of CIKS activity has been shown to prevent and alleviate pathological symptoms in an animal model of rheumatoid arthritis and multiple sclerosis, and it is hypothesized that disruption of the interaction between CIKS and TRAF6 is a therapeutic strategy for the selective prevention of certain IL-17-mediated diseases.
NIAID investigators have discovered a short sequence within CIKS that is responsible for CIKS interaction with TRAF6. The disclosed sequence can be used to develop blocking peptides for the treatment of IL-17-mediated autoimmune diseases, inflammatory diseases, and cancers.
Applications:
Therapeutics for IL-17-mediated diseases, such as inflammatory diseases, autoimmune diseases, and cancer
Advantages:
Selective inhibition of CIKS-TRAF6 interactions
Development Status:
Basic research
Inventors:
Ulrich Siebenlist (NIAID)
Soeren U Soender (NIAID)
Sun Saret (NIAID)
Patent Status:
HHS, Reference No. E-268-2010/0
US, Application No. 61/418,782 filed 01 Dec 2010
Relevant Publication:
Licensing Status:
Available for licensing
Portfolios:
Cancer
Cancer - Therapeutics
Internal Medicine
Internal Medicine - Therapeutics
For Licensing Information Please Contact:
Tara Kirby Ph.D.
NIH Office of Technology Transfer
6011 Executive Blvd. Suite 325,
Rockville, MD 20852
United States
Email: tk200h@nih.gov
Phone: 301-435-4426
Fax: 301-402-0220
Ref No: 2236
Updated: 03/2011