Aclidinium Bromide

For research use only.

Catalog No.S4031 Synonyms: LAS 34273, LAS-W 330

Aclidinium Bromide Chemical Structure

Molecular Weight(MW): 564.55

Aclidinium Bromide inhibits human muscarinic AChR M1, M2, M3, M4 and M5 with Ki of 0.1 nM, 0.14 nM, 0.14 nM, 0.21 nM and 0.16 nM, respectively.

Size Price Stock Quantity  
10mM (1mL in DMSO) USD 220 In stock
USD 170 In stock
USD 970 In stock
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Biological Activity

Description Aclidinium Bromide inhibits human muscarinic AChR M1, M2, M3, M4 and M5 with Ki of 0.1 nM, 0.14 nM, 0.14 nM, 0.21 nM and 0.16 nM, respectively.
Features Approximately equipotent to Tiotropium, and 8-16 times more potent than Ipratropium for muscarinic receptor subtypes.
M1 mAChR [1] M2 mAChR [1] M3 mAChR [1] M5 mAChR [1] M4 mAChR [1]
0.1 nM(Ki) 0.14 nM(Ki) 0.14 nM(Ki) 0.16 nM(Ki) 0.21 nM(Ki)
In vitro

[3H]Aclidinium binds to a homogeneous receptor of M2 with Kd of 0.34 nM and Bmax of 3.13 pmol/mg, and binds to M3 with Kd of 0.34 nM and Bmax of 3.13 pmol/mg. Aclidinium (< 100 nM) dose-dependently inhibits carbachol-induced contractions in isolated guinea pig trachea. Aclidinium shows an onset of action with t1/2 of 6.8 min, tmax of 35.9 min in isolated guinea pig trachea. [1] Aclidinium is hydrolysed in plasma samples from all species studied, with apparent half-lives at 37℃ of 11.7 min, 38.3 min, 1.8 min and 2.4 min in rat, guinea pig, dog and human plasma, respectively. [2] Aclidinium (0.1 μM) inhibits carbachol and TGF-β1 induced upregulation of collagen type I and α-SMA mRNA and protein expression in human bronchial fibroblasts. Aclidinium (0.1 μM) inhibits TGF-β1 induced upregulation of ChAT expression in human bronchial fibroblasts. Aclidinium (0.1 μM) inhibits carbachol- and TGF-β1-induced increases in ERK1/2 phosphorylation and RhoA-GTP formation in human bronchial fibroblasts. Aclidinium pretreatment prevents the upregulation of M1 and M3, but not M2 downregulation induced by carbachol or TGF-β1 in human lung fibroblasts. Aclidinium (0.1 μM) dose-dependently inhibits the TGF-β1 and carbachol-induced cell proliferation of human lung fibroblasts. [3]

In vivo Aclidinium shows an onset of action with IC50 (95% CI) of 140 μg/mL and tmax of 30 min in the acetylcholine-induced bronchoconstriction model in anesthetized guinea pigs. Aclidinium (500 μg/kg) induces a maximal increase in heart rate of 55% after 1 hour in conscious beagle dogs. [1] Aclidinium (1 mg/ml) produces a potent and sustained bronchoprotection (72%–88.4%) over the 120-min study period in anaesthetised guinea pigs. [2]


Kinase Assay:[1]
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Affinity assay:

The affinity of Aclidinium for the different human muscarinic receptor subtypes at equilibrium is determined by measuring their ability to displace the binding of [3H]NMS to cell membrane preparations expressing one of the human muscarinic receptor subtypes. Protein concentrations are 8.1 μg/well, 10.0 μg/well, 4.9 μg/well, 4.5 μg/well, and 5.0 μg/well for M1, M2, M3, M4, and M5 receptor membrane preparations, respectively. The assays are conducted at [3H]NMS concentrations approximately equal to the radioligand equilibrium dissociation constant (Kd) for the different muscarinic receptors subtypes. The [3H]NMS concentration is 0.3 nM for the M1 and M4 assays and 1 nM for the M2, M3, and M5 assays. A range of antagonist concentrations (10−14 to 10−5 M) are tested in duplicate to generate competition curves. Nonspecific binding is determined in the presence of atropine (1 μM). Assay reagents are dissolved in assay binding buffer (phosphate-buffered saline with calcium and magnesium) to a total volume of 200 μL. After a 2 hours or 6 hours incubation period (M1–M4 and M5, respectively) at room temperature in 96-well microtiter plates to ensure that equilibrium is achieved for Aclidinium, 150 μL aliquots of the reaction are transferred to GF/C filter plates pretreated for 1 hour with wash buffer (50 mM Tris, 100 mM NaCl, pH 7.4) containing 0.05% polyethylenimine. Bound and free [3H]NMS are then separated by rapid vacuum filtration followed by four washes with ice-cold wash buffer. Filters are then dried for 30 min before addition of 30 μL of OptiPhase Supermix, and radioactivity is quantified using a MicroBeta Trilux microplate scintillation counter.
Cell Research:[3]
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  • Cell lines: Human bronchial fibroblast
  • Concentrations: 100 nM
  • Incubation Time: 48 hours
  • Method: Human bronchial fibroblast proliferation is measured as previously outlined by colorimetric immunoassay based on BrdU incorporation during DNA synthesis using a cell proliferation enzyme-linked immunosorbent assay BrdU kit according to the manufacturer’s protocol. Cells are seeded at a density of 3x103 cells/well on 96-well plates and incubated for 24 hours. Cells are then exposed to different experimental conditions. The 490 nm absorbance is quantified using a microplate spectrophotometer. Proliferation data refers to the absorbance values of BrdU-labeled cellular DNA content per well. Stimulation is expressed as x-fold proliferation over basal growth of the untreated control set as unity.
    (Only for Reference)
Animal Research:[1]
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  • Animal Models: beagle dogs
  • Dosages: 500 μg/kg
  • Administration: Administered by using a nebulizer
    (Only for Reference)

Solubility (25°C)

In vitro DMSO 113 mg/mL (200.15 mM)
Water Insoluble
Ethanol Insoluble
In vivo Add solvents to the product individually and in order(Data is from Selleck tests instead of citations):
30% PEG400+0.5% Tween80+5% propylene glycol
For best results, use promptly after mixing.
30 mg/mL

* Please note that Selleck tests the solubility of all compounds in-house, and the actual solubility may differ slightly from published values. This is normal and is due to slight batch-to-batch variations.

Chemical Information

Molecular Weight 564.55


CAS No. 320345-99-1
Storage powder
in solvent
Synonyms LAS 34273, LAS-W 330
Smiles [Br-].OC(C(=O)OC1C[N+]2(CCCOC3=CC=CC=C3)CCC1CC2)(C4=CC=CS4)C5=CC=CS5

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AChR Signaling Pathway Map

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Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID