Disease relevance of ICI 200355

• ICI 200,355 had no effect on baseline secretion or on the secretory response to chymase, cathepsin G or Pseudomonas aeruginosa elastase [1].
• Thus, ICI 200,355 appears to be a useful tool for investigating the role of human neutrophil elastase in inflammatory disorders associated with hypersecretion, such as cystic fibrosis, chronic bronchitis, and asthma [1].

High impact information on ICI 200355

• We have obtained identical results with alpha1-antitrypsin, alpha2m, recombinant secretory leukocyte proteinase inhibitor, and ICI 200,355, and we have found that phagocyte-derived oxidants are not required for the genesis of this catalytic activity [2].
• ICI 200,355, a selective inhibitor of neutrophil elastase, prevented LTB(4)-induced nasal secretion and lysozyme secretion, but it had no effect on neutrophil recruitment [3].
• Pretreatment with the selective neutrophil elastase inhibitor ICI 200,355 also prevented ovalbumin-induced goblet cell degranulation, implicating elastase [4].
• RESULTS--When preincubated with neutrophils both rSLPI and r alpha 1-PI were effective inhibitors of fibronectin degradation although n alpha 1-PI and ICI 200,355 were less effective [5].
• This effect was largely (83%; P<0.02) inhibited by ICI 200,355, a specific inhibitor of neutrophil elastase [6].

Biological context of ICI 200355

• ICI 200,355 produced a concentration-dependent inhibition of the secretory response induced by human neutrophil elastase (10(-8) M), with an IC50 of 1.6 x 10(-8) M [1].

Anatomical context of ICI 200355

• Both alpha1-PI and ICI 200,355 inhibited the activity of elastase obtained from stimulated ovine neutrophils [7].
• Addition of the selective neutrophil elastase inhibitor ICI 200,355 inhibited the secretory response to CF sputum supernatant by 89% [8].

Associations of ICI 200355 with other chemical compounds

• Biologic characterization of ICI 200,880 and ICI 200,355, novel inhibitors of human neutrophil elastase [9].

Gene context of ICI 200355

• ICI 200,355 also inhibited the ongoing destruction of insoluble elastin by human neutrophil elastase [1].
• ICI 200,355 (an inhibitor of neutrophil elastase and proteinase-3) or secretory leukocyte protease inhibitor (an inhibitor of elastase but not of proteinase-3) abolished IL-8-induced GC degranulation, implicating elastase [10].
• The combination of aprotinin, an inhibitor of cathepsin G, and ICI 200,355 caused significantly more reduction in the secretory response than ICI 200,355 alone (89.12 +/- 3.8 versus 72.53 +/- 5.89% reduction, p < 0.05) [11].

References