- 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
- October 9, 2014 - Safety, Tolerability, and Pharmacokinetics of the Oral S-Nitrosoglutathione Reductase Inhibitor N91115: A Multiple Ascending-Dose Study In Healthy Subjects
- October 9, 2014 - Safety, Tolerability, and Pharmacokinetics of the Intravenous S-NitrosoglutathioneReductaseInhibitor N6022: An Ascending-Dose Study in Subjects Homozygous for the F508del-CFTRMutation
- October 4, 2014 - Pharmacological Correction and Acute Inhibition of GSNOR Results in Improved In Vitro CFTR Function
- October 4, 2014 - Neutrophil Elastase-Mediated CFTR Damage is Rescued by Intracellular Bioavailable GSNO
- March 21, 2014 - Primary airway epithelial cells expanded with feeder cells and ROCK inhibitor for screening novel GSNOR inhibitors and CFTR correctors
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March 21, 2014 Primary airway epithelial cells expanded with feeder cells and ROCK inhibitor for screening novel GSNOR inhibitors and CFTR correctors
Peter F. Bove, Kirsten M. Look, Michael A. Suniga, Xicheng Sun, and Sherif E. Gabriel
The current cell culture technology limits our ability to indefinitely expand primary human airway epithelial (HAE) cells while retaining their cell-specific phenotype and function. Controlled experiments of primary non-CF and cystic fibrosis (CF)-derived HAE cells determined that they retain primary culture morphology and functional properties for only a few passages (up to passage 2), thereby limiting the number of critical in vitro experiments performed.
Therefore, the ability to markedly increase the supply of functionally relevant primary HAE cells derived from patients with various CF mutations (i.e. ΔF508, G551D, R117H, etc.) will allow for a significant increase in additional future studies designed to evaluate essential therapeutics for mutation specific CFTR correction or potentiation. More…(655 Kb)
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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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