Elastase Inhibitors

The present Competitive Intelligence Report about elastase inhibitors provides a competitor evaluation in the field of human plasma-derived, recombinant, transgenic, synthetic and gene therapeutic approaches for treatment of lung emphysema caused by congenital deficiency of antitrypsin or for treatment of chronic obstructive pulmonary disease (COPD) as of May 2009. Neutrophil elastase (NE) is a serine protease, expressed mainly by neutrophils, that is capable of degrading a variety of structural proteins of the extracellular matrix.

Infiltration of activated neutrophils and excessive NE activity have been implicated in several lung diseases, including acute lung injury, cystic fibrosis, pulmonary fibrosis and COPD. Thus, a NE inhibitor targeting excessive NE activity in lung tissue could have good therapeutic potential.

Endogenous human neutrophil elastase is predominantly neutralized by alpha-1 antitrypsin (AAT), also called alpha-1 proteinase inhibitor (alpha1-PI). Congenital deficiency of AAT leads to emphysema which can be treated by substitution with therapeutic AAT. At present, alpha-1 antitrypsin products are human plasma-derived purified products. Recombinant AAT products are under development. Neutrophil elastase also has attracted much interest as a target for inhibition to treat chronic obstructive pulmonary disease (COPD), asthma and other inflammatory disease conditions. Synthetic and recombinant elastase inhibitors have been identified and are in clinical and preclinical development.

The report includes a compilation of current active products and projects in research and development of human neutorphil elastase targeting small molecules, purified and recombinant proteins and DNA. In addition, the report lists company-specific R&D pipelines of elastase targeting molecules. Competitor projects are listed in a tabular format providing information on - Drug Codes, - Target / Mechanism of Action, - Class of Compound, - Company, - Product Category, - Indication, - R&D Stage and - additional comments with a hyperlink leading to the source of information.