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TIP60 inhibitors – therapy for Irritable Bowel Disease (IBD); ulcerative colitis and Crohn’s diseases

Inhibitors of TIP60, maintaining regulatory T cells (Tregs) and ameliorating autoimmune diseases.


Inflammatory bowel disease (IBD) involves chronic inflammation of all or part of digestive tract. IBD includes ulcerative colitis and Crohn’s disease both very prevalent and known to cause severe complications and discomfort.

Inhibitors of TIP60, a histone acetyltransferase, have been developed to maintain peripheral Treg cells, further enabling them to ameliorate autoimmune diseases. Preliminary animal studies have focused on the treatment of colitis, but these compounds are expected to find application in a wide variety of autoimmune disorders.  


Dr. Greene’s laboratory synthesized small molecules that bind and modulate TIP60 acetyltransferase activity. Lead compounds tested bind to TIP60’s non-active site while maintaining its scaffolding ability. As a result, TIP60 binds FOXP3 and recruits p300, leading to FOXP3’s increased overall transcriptional activity and positive regulation of Treg cells. Since the deficiency or dysfunction of Treg cells has been linked to several autoimmune and inflammatory diseases including IBD, increasing their function through functional inhibition of TIP60 directly points to potential therapeutic approach. 


  • TIP60 inhibition as a novel pathway to treat for autoimmune diseases.
  • Potential therapy for a wide range of therapies as TIP60 is involved in mediating activities of T regulatory cells, which in turn play an important role in autoimmune and inflammatory diseases.


In vivo animal data demonstrates POC efficacy in treating ulcerative colitis.

Stage of Development: 

Animal studies have been completed and positive results reported where TIP60 inhibitor therapy reversed weight loss, blood in the stool and diarrhea, as well as maintained colon length.

Intellectual Property: 

USSN 9,701,631 

Reference Media: 

Desired Partnerships: 

Patent Information:


Docket # X5743

For Information, Contact:

Viviane Martin
University of Pennsylvania