- 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
- August 27, 2012 - N30 Pharma Converts from LLC to C-Corp
- February 21, 2012 - Board Adds Evan Loh, MD and John R. Moore
- March 21, 2013 - S-nitrosoglutathione Reductase Inhibitors Modulate F508-del CFTR Protein Levels and Chloride Secretion In Vitro
- March 20, 2013 - Small Molecule Inhibitors of GSNOR Possess Anti-Inflammatory and Bronchodilatory Actions in Mouse Models of Inflammatory Lung Disease and Modulate CFTR Function in F508del-CFTR Mice
- November 11, 2011 - S-Nitrosoglutathione Reductase Inhibitors for the Prevention and Treatment of Experimental Colitis
- August 28, 2011 - Structure – Activity Relationships of Pyrrole Based S-Nitrosoglutathione Reductase Inhibitors – Carboxamide Modification
- July 14, 2011 - Heterozygous Deletion of S-Nitrosoglutathione Reductase in Mice Does Not Increase Nitrosative Inactivation of O6-Alkylguanine-DNA Alkyltransferase or Diethylnitrosamine-induced Hepatocarcinogenesis
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Home  N30 Pharmaceuticals Boulder Colorado headquarters N30 Pharmaceuticals
Founded in 2007 with headquarters in Boulder, Colorado.
N30 Pharma is developing a novel class of disease modifying therapies that preserve intracellular GSNO (S-nitrosoglutathione), a key regulator of organ repair, regeneration, and healing. The Company’s lead program is focused on cystic fibrosis.
As the body’s primary reservoir of nitric oxide (NO), GSNO plays a pivotal role in NO signaling. Decreased GSNO levels are associated with inflammatory lung disease, and with increased activity of GSNOR (GSNO reductase), the primary catabolizing enzyme of GSNO.
N30 Pharma has developed a broad portfolio of proprietary, potent, small molecule inhibitors of GSNOR that have been shown to preserve endogenous GSNO levels and to be effective in “gold-standard” models of inflammatory lung disease.
Cystic Fibrosis
- Reduced levels of GSNO are associated with cystic fibrosis
- GSNO, through nitric oxide signaling, is integral to the normal function of CFTR, the transmembrane regulator protein that is defective in cystic fibrosis
- Anti-inflammatory effects of GSNOR inhibitors relevant to cystic fibrosis include decreased NFκB activation, neutrophilic infiltration, and elastase-mediated lung injury
- Lead compound, N6022, has completed Phase 1 testing in healthy subjects, a proof of concept study in asthma, and is poised to enter clinical trials in cystic fibrosis in the first quarter of 2013
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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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