Therapeutic Approach for Autoimmune Diseases, Inflammatory Diseases and Cancers by Blocking CIKS-TRAF6 Interactions

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.

Potential Commercial Applications: Competitive Advantages:
Therapeutics for IL-17-mediated diseases, such as inflammatory diseases, autoimmune diseases, and cancer   Selective inhibition of CIKS-TRAF6 interactions

Ulrich Siebenlist (NIAID)
Soeren Soender (NIAID)
Sun Saret (NIAID)

Intellectual Property:
PCT Application No. PCT/US2011/062945
US Application No. 61/418,782

Pisitkun P, et al. (2010) PubMed: 20662069
Claudio E, et al. (2009) PubMed: 19155511

Licensing Contact:
Jaime Greene , M.S.
NIH Office of Technology Transfer
Phone: 301-435-5559

OTT Reference No: E-268-2010/0

Updated: Mar-15-2011