My cart
In the shopping cart is not goods, to choose and buy!
  • Product Name
  • Size
  • Quantity
  • Amount
    Selected items : 0 pieces Total : CHECK OUT()
    Aclidinium Bromide (LAS 34273; LAS-W 330)
    Aclidinium Bromide (LAS 34273; LAS-W 330)

    Price:
    Market Price:

    This product is for research use only, not for human use. We do not sell to patients.
    Number: - + Pieces(InventoryPieces)
    InvivoChem Cat #: V1194
    CAS #: 320345-99-1Purity ≥98%

    Description: Aclidinium Bromide (formerly LAS34273, LAS-W 330; brand names Tudorza Genuair; Eklira Genuair; Bretaris Genuair) is a potent, long-acting and inhalable muscarinic antagonist used as a maintenance treatment for chronic obstructive pulmonary disease (COPD). It acts by potently inhibiting human muscarinic acetylcholine receptors-AChR M1, M2, M3, M4 and M5 with Ki values of 0.1 nM, 0.14 nM, 0.14 nM, 0.21 nM and 0.16 nM, respectively.  

    References: J Pharmacol Exp Ther. 2009 Nov;331(2):740-51; Eur J Pharm Sci. 2010 Mar 18;39(5):283-90. 

    Customer Validation
    Official Supplier of
    • VE
    • OF
    • YALE
    • hhmi
    • 香港大学
    Related Products
    Publications Citing InvivoChem Products
    • Physicochemical and Storage Information
    • Protocol
    • Quality Control Documentation
    • Related Biological Data
    • Customer Review
    Molecular Weight (MW)564.55 
    FormulaC26H30NO4S2.Br 
    CAS No.320345-99-1 
    Storage-20℃ for 3 years in powder form
    -80℃ for 2 years in solvent
    Solubility (In vitro)DMSO: 113 mg/mL (200.15 mM)
    Water: <1 mg/mL
    Ethanol: <1 mg/mL 
    Solubility (In vivo)30% PEG400+0.5% Tween80+5% Propylene glycol:  30 mg/mL 
    SynonymsLAS 34273, LAS W 330; LAS-34273, LAS-W 330; LAS34273, LASW 330; trade name: Eklira Genuair; Tudorza Genuair; Bretaris Genuair


    • Molarity Calculator
    • Dilution Calculator
    • The molarity calculator equation

      Mass (g) = Concentration (mol/L) × Volume (L) × Molecular Weight (g/mol)

      • Mass
      • Concentration
      • Volume
      • Molecular Weight *
      • =
      • ×
      • ×
    • The dilution calculator equation

      Concentration (start) × Volume (start) = Concentration (final) × Volume (final)

      This equation is commonly abbreviated as: C1V1 = C2V2

      • Concentration (start)
      • ×
      • Volume (start)
      • =
      • Concentration (final)
      • ×
      • Volume (final)
      • ×
      • =
      • ×
      • C1
      •  
      • V1
      •  
      • C2
      •  
      • V2
    In Vitro

    In vitro activity: [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. 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. 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.


    Kinase 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 Assay: 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.

    In VivoAclidinium 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. Aclidinium (1 mg/ml) produces a potent and sustained bronchoprotection (72%–88.4%) over the 120-min study period in anaesthetised guinea pigs. 
    Animal modelBeagle dogs 
    Formulation & DosagePrepared as Aerosol solutions; 500 μg/kg; administered through a nebulizer
    References

    J Pharmacol Exp Ther. 2009 Nov;331(2):740-51; Eur J Pharm Sci. 2010 Mar 18;39(5):283-90. 


    These protocols are for reference only. InvivoChem does not independently validate these methods.

    Aclidinium Bromide

    Duration of action of inhaled aclidinium, ipratropium, and tiotropium in the acetylcholine-induced bronchoconstriction model in guinea pigs. J Pharmacol Exp Ther. 2009 Nov;331(2):740-51. 
     

    Aclidinium Bromide

    Effects of aclidinium and tiotropium on acetylcholine-induced bronchoconstriction in anesthetized beagle dogs. J Pharmacol Exp Ther. 2009 Nov;331(2):740-51. 
     
    Aclidinium Bromide
    Effect of aclidinium and tiotropium on heart rate in conscious beagle dogs. J Pharmacol Exp Ther. 2009 Nov;331(2):740-51. 


    评论

      Home Prev Next Last page / pices

      发评论

      ×
      Your information is safe with us. * Required Fields.
      Products are for research use only;  We do not sell to patients
      Tel: 1-708-310-1919
      Fax: 1-708-557-7486
      Subscribe to our E-newsletter
      • Name*
      • *
      • E-mail*
      • *
      • instructions:
      • *
      Copyright 2020 InvivoChem LLC | All Rights Reserved
      prompt
      Do you confirm the receipt?