BOULDER, Colo.--(BUSINESS WIRE)--miRagen Therapeutics, Inc., a biopharmaceutical company developing innovative microRNA-based therapeutics, announced today that findings from a research collaboration between the Company and Yale University have demonstrated that promiR-29 reversed fibrosis in a mouse model of pulmonary fibrosis. These findings were published in the journal EMBO Molecular Medicine http:\/\/onlinelibrary.wiley.com\/doi\/10.15252\/emmm.201303604\/full<\/a> on September 19, 2014. <\/p>\n The mimic, when injected into the blood, goes to the lung and it has a sustained effect. We are very impressed that it can reverse fibrosis, not only prevent it, said Naftali Kaminski, M.D., a professor at Yale School of Medicine and section chief of pulmonary, critical care and sleep medicine and a corresponding author of the study. <\/p>\n Results from the collaborative research conducted by miRagen and Yale have led to the award of a Centers for Advanced Diagnostics and Experimental Therapeutics in Lung Diseases Stage II grant from the National Institutes of Health to further evaluate this potential therapeutic approach. <\/p>\n miRagen is committed to translating these pre-clinical findings into transformative therapies for patients with Idiopathic Pulmonary Fibrosis, said Dr. David Rodman, Executive Vice President of Research and Development at miRagen Therapeutics, Inc. We are excited about the collaboration with Dr. Kaminski and by the potential for accelerated progression to human clinical trials afforded by the CADET II grant award. <\/p>\n About microRNAs <\/p>\n MicroRNAs have emerged as an important class of small RNAs encoded in the genome, acting as master regulators of gene expression. Recent studies have indicated that microRNAs appear to be associated with many disease processes. Because they are thought to be single molecular entities that dictate the expression of fundamental regulatory pathways, microRNAs represent potential drug targets for controlling many biologic and disease processes.1 <\/p>\n About microRNA-29 <\/p>\n The microRNA-29 family is a well-established regulator of extracellular matrix genes. The expression of the three family members is consistently down-regulated in a number of pathological fibrotic conditions, including cardiac, renal, hepatic, and pulmonary fibrosis, as well as systemic sclerosis2,3,4,5. Numerous studies in cell-culture and genetic replacement in rodents have also demonstrated the potential of miR-29 normalization to correct many drivers of pathological fibrosis. <\/p>\n About miRagen Therapeutics, Inc. <\/p>\n miRagen Therapeutics, Inc., is a biopharmaceutical company focused on the discovery and development of innovative microRNA (miRNA)-targeting therapies in disease areas of high unmet medical need. The Company seeks to leverage in-house expertise in miRNA biology, oligonucleotide chemistry, and drug development to evaluate and advance promising technologies and high-potential product candidates for its own pipeline and in conjunction with strategic collaborators. For certain cardiovascular disease programs, miRagen has a collaboration and license agreement with Servier, an independent French research-based pharmaceutical company. miRagen retains all rights for the Servier-partnered programs in the U.S. and Japan. For more information, please visit http:\/\/www.miragenrx.com<\/a>. <\/p>\n <\/p>\n See the original post here:<\/p>\n Research Findings Demonstrate miRagen Therapeutics Synthetic microRNA-29 Mimic (promiR-29) Reverses Pulmonary Fibrosis<\/a><\/p>\n","protected":false},"excerpt":{"rendered":" BOULDER, Colo.--(BUSINESS WIRE)--miRagen Therapeutics, Inc., a biopharmaceutical company developing innovative microRNA-based therapeutics, announced today that findings from a research collaboration between the Company and Yale University have demonstrated that promiR-29 reversed fibrosis in a mouse model of pulmonary fibrosis. These findings were published in the journal EMBO Molecular Medicine http:\/\/onlinelibrary.wiley.com\/doi\/10.15252\/emmm.201303604\/full<\/a> on September 19, 2014 Continue reading