USPTO allows Regulus Therapeutics' claims covering methods of antagonizing miR-181a for regulating immune response

Regulus Therapeutics Inc. announced today that the United States Patent and Trademark Office (USPTO) has allowed claims in U.S. Application Serial No. 11/977,506 covering methods of antagonizing miR-181a to regulate immune response. This patent is owned by Stanford University and licensed exclusively to Regulus. miR-181a has been shown to regulate the response of immune cells, such as T lymphocytes, to specific stimuli and modulation of miR-181a could lead to a novel treatment of inflammatory disease.

“More broadly, we continue to build a robust patent portfolio that supports our strategy of developing and commercializing high-impact microRNA-based therapeutics in multiple disease areas.”

“We are pleased with the decision of the USPTO to allow this first application based on the Li et al. patent filing. We are applying our expertise in microRNA biology and nucleic acid chemistry to develop novel medicines for treating inflammatory disease, and this new allowance will expand the scope of our exclusivity surrounding the anti-miR approach to miR-181a,” said Garry E. Menzel, Ph.D., Executive Vice President of Corporate Development and Finance of Regulus Therapeutics. “More broadly, we continue to build a robust patent portfolio that supports our strategy of developing and commercializing high-impact microRNA-based therapeutics in multiple disease areas.”

Data published in 2007 by scientists at Stanford University and Alnylam Pharmaceuticals in the journal Cell [Li QJ et al. 2007 Apr. 6;129(1):147-61] demonstrated that modulation of miR-181a levels in an immune cell modified the sensitivity of the cell to specific stimuli. Increased expression of miR-181a led to an increase in immune cell response to an inflammatory stimulus. Conversely, decreasing levels of miR-181a in immune cells de-sensitized the cell to the stimulus. Consistent with this observation, using an anti-miR to antagonize miR-181a function reduced immune cell response to a stimulus.

The newly allowed claims cover methods of modulating miR-181a in T cells, to raise the T cell receptor signaling threshold, and decrease the sensitivity of T cells to antigen stimulation. The claims cover the use of a broad class of anti-miRs targeting miR-181a, including anti-miRs having varying lengths and chemical modifications.