- March 12, 2014 - N30 Announces Start of Oral Dosing of N91115 in a Phase 1 Clinical Trial
- October 15, 2013 - N30 Announces Presentations at the 2013 North American Cystic Fibrosis Conference
- April 2, 2013 - N30 Announces Presentation of Preclinical Data at the Basic Science Meeting of the European Cystic Fibrosis Society
- March 13, 2013 - N30 Announces First Patient Treated in Clinical Trial of N6022 in Cystic Fibrosis
- October 8, 2012 - N30 Names Sherif Gabriel, Ph.D. as VP Research
- March 21, 2014 - Primary airway epithelial cells expanded with feeder cells and ROCK inhibitor for screening novel GSNOR inhibitors and CFTR correctorsPrimary airway epithelial cells expanded with feeder cells and ROCK inhibitor for screening novel GSNOR inhibitors and CFTR correctors
- March 21, 2014 - Identification of Novel, Efficacious F508del‐CFTR Correctors to Treat Cystic Fibrosis
- October 14, 2013 - Next generation F508del CFTR correctors using a YFP based high throughput screening assay
- October 14, 2013 - Intestinal Current Measurement to Assess Modulation of F508del-CFTR Function
- October 14, 2013 - A Novel GSNOR Inhibitor with Potent Bronchodilatory Effects and CFTR Potentiation Activity
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March 11, 2011 Discovery of S-Nitrosoglutathione Reductase Inhibitors: Potential Agents for the Treatment of Asthma and Other Inflammatory Diseases
Xicheng Sun, Jan W. F. Wasley, Jian Qiu, Joan P. Blonder, Adam M. Stout, Louis S. Green, Sarah A. Strong, Dorothy B. Colagiovanni, Jane P. Richards, Sarah C. Mutka, Lawrence Chun, and Gary J. Rosenthal
S-Nitrosoglutathione reductase (GSNOR) regulates S-nitrosothiols (SNOs) and nitric oxide (NO) in vivo through catabolism of S-nitrosoglutathione (GSNO). GSNOR and the anti-inflammatory and smooth muscle relaxant activities of SNOs, GSNO, and NO play significant roles in pulmonary, cardiovascular, and gastrointestinal function. In GSNOR knockout mice, basal airway tone is reduced and the response to challenge with bronchoconstrictors or airway allergens is attenuated. Consequently, GSNOR has emerged as an attractive therapeutic target for several clinically important human diseases. As such, small molecule inhibitors of GSNOR were developed.
These GSNOR inhibitors were potent, selective, and efficacious in animal models of inflammatory disease characterized by reduced levels of GSNO and bioavailable NO. N6022, a potent and reversible GSNOR inhibitor, reduced bronchoconstriction and pulmonary inflammation in a mouse model of asthma and demonstrated an acceptable safety profile.
N6022 is currently in clinical development as a potential agent for the treatment of acute asthma.
ACS Med. Chem. Lett. 2011, 2, 402–406. (More…Pubs ACS website) 
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- January 24, 2013 - Pharmacological Inhibition of S-Nitrosoglutathione Reductase Improves Endothelial Vasodilatory Function in Rats in vivo
- December 28, 2012 - ADH IB Expression, but Not ADH III, Is Decreased in Human Lung Cancer
- February 15, 2012 - Mechanism of Inhibition for N6022, a First-in-Class Drug Targeting GSNOR
- January 13, 2012 - Structure–activity relationship of pyrrole based GSNOR inhibitors
- August 25, 2011 - Preclinical 28-Day Inhalation Toxicity Assessment of S-Nitrosoglutathione
- July 26, 2011 - Discovery of potent and novel GSNOR inhibitors devoid of cytochrome P450 activities
- April 19, 2011 - Structure–activity relationships of pyrrole based GSNOR inhibitors: Pyrrole regioisomers and propionic acid replacement
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