Aclidinium Bromide - CAS 320345-99-1
Not Intended for Therapeutic Use. For research use only.
Category:
Inhibitor
Product Name:
Aclidinium Bromide
Catalog Number:
320345-99-1
Synonyms:
trade name: Eklira Genuair; Tudorza Genuair; Bretaris Genuair
CAS Number:
320345-99-1
Description:
Aclidinium Bromide(LAS 34273; LAS-W 330) is a long-acting, inhaled muscarinic antagonist as a maintenance treatment for chronic obstructive pulmonary disease (COPD).
COA:
Inquire
MSDS:
Inquire
Targets:
mAChR
Chemical Structure
CAS 320345-99-1 Aclidinium Bromide

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Reference Reading


1.Faster reduction in hyperinflation and improvement in lung ventilation inhomogeneity promoted by aclidinium compared to glycopyrronium in severe stable COPD patients. A randomized crossover study.
Santus P1, Radovanovic D2, Di Marco F3, Raccanelli R4, Valenti V5, Centanni S6. Pulm Pharmacol Ther. 2015 Dec;35:42-9. doi: 10.1016/j.pupt.2015.11.001. Epub 2015 Nov 6.
Standard spyrometric assessment in chronic obstructive pulmonary disease (COPD) only evaluates bronchial obstruction. However, airflow limitation and hyperinflation are the main pathophysiological factors responsible for dyspnoea and reduced exercise tolerance in patients with COPD. This study evaluated the effects of aclidinium bromide 400 μg and glycopyrronium bromide 50 μg on these parameters. Patients with stable severe/very severe COPD were randomized in this double-blind, double-dummy, crossover, Phase IV study. Patients received single doses of each drug on separate days. Primary endpoints were changes in residual volume (RV) and intra-thoracic gas volume (ITGV), assessed by full-body plethysmography. Other endpoints included changes variations in lung ventilation inhomogeneity (Phase III slope of single-breath nitrogen washout test, SBN2), dyspnoea visual analogue scale, and pulmonary specific total airway resistances. Assessments were performed at baseline and 5, 15, 30, 60, and 180 min post-administration.
2.Aclidinium bromide combined with formoterol inhibits remodeling parameters in lung epithelial cells through cAMP.
Lambers C1, Costa L2, Ying Q2, Zhong J2, Lardinois D3, Dekan G4, Schuller E5, Roth M6. Pharmacol Res. 2015 Dec;102:310-8. doi: 10.1016/j.phrs.2015.09.010. Epub 2015 Nov 4.
Combined muscarinic receptor antagonists and long acting β2-agonists improve symptom control in chronic obstructive pulmonary disease (COPD) significantly. In clinical studies aclidinium bromide achieved better beneficial effects than other bronchodilators; however, the underlying molecular mechanisms are unknown. This study assessed the effect of aclidinium bromide combined with formoterol on COPD lung (n=20) and non-COPD lung (n=10) derived epithelial cells stimulated with TGF-β1+carbachol on: (i) the generation of mesenchymal cells in relation to epithelial cells, (II) extracellular matrix (ECM) deposition, and (iii) the interaction of ECM on the generation of epithelial and mesenchymal cells. TGF-β1+carbachol enhanced the generation of mesenchymal cells, which was significantly reduced by aclidinium bromide or formoterol. The effect of combined drugs was additive. Inhibition of p38 MAP kinase and Smad by specific inhibitors or aclidinium bromide reduced the generation of mesenchymal cells.