Fenoterol HBr - CAS 1944-12-3
Catalog number:
Not Intended for Therapeutic Use. For research use only.
Molecular Formula:
C17H21NO4. HBr
Molecular Weight:
Adrenergic Receptor
Fenoterol hydrobromide is a β2-adrenergic agonist agent used for asthma and chronic obstructive pulmonary disease treatment. It has already been approved for use.
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Fenoterol Hydrobromide; 5-[1-Hydroxy-2-[[2-(4-hydroxyphenyl)-1-methylethyl]amino]ethyl]-1,3-benzenediol Hydrobromide;
DMSO: ≥ 38 mg/mL
-20°C Freezer
Fenoterol hydrobromide is useful in the treatment of asthma and chronic obstructive pulmonary disease as a β2-adrenergic agonist agent.
Shelf Life:
As supplied, 2 years from the QC date provided on the Certificate of Analysis, when stored properly
Melting Point:
226-230 °C
Canonical SMILES:
Current Developer:
Boehringer Ingelheim
1.β2-adrenoceptor agonist-evoked reactive oxygen species generation in mouse atria: implication in delayed inotropic effect.
Odnoshivkina UG1, Sytchev VI1, Nurullin LF2, Giniatullin AR1, Zefirov AL1, Petrov AM3. Eur J Pharmacol. 2015 Oct 15;765:140-53. doi: 10.1016/j.ejphar.2015.08.020. Epub 2015 Aug 20.
Fenoterol, a β2-adrenoceptor agonist, has anti-apoptotic action in cardiomyocytes and induces a specific pattern of downstream signaling. We have previously reported that exposure to fenoterol (5 μM) results in a delayed positive inotropic effect which is related to changes in both Ca2+ transient and NO. Here, the changes in reactive oxygen species (ROS) production in response to the fenoterol administration and the involvement of ROS in effect of this agonist on contractility were investigated in mouse isolated atria. Stimulation of β2-adrenoceptor increases a level of extracellular ROS, while intracellular ROS level rises only after removal of fenoterol from the bath. NADPH-oxidase inhibitor (apocynin) prevents the increase in ROS production and the Nox2 isoform is immunofluorescently colocalized with β2-adrenoceptor at the atrial myocytes. Treatments with antioxidants (N-acetyl-L-cysteine, NADPH inhibitors, exogenous catalases) significantly inhibit the fenoterol induced increase in the contraction amplitude, probably by attenuating Ca2+ transient and up-regulating NO production.
2.Have we achieved progress in tocolytic treatment?--results of a retrospective cohort study in a tertiary university hospital.
Tomczyk K, Rzymski P, Wilczak M. Ginekol Pol. 2015 Jul;86(7):504-8.
OBJECTIVES: Beta-agonists play an important role in tocolytic treatment. In light of recent changes in the Polish medical care system, we decided to assess the effectiveness of oral continuous treatment (in 2012) and compare it with a 3-day intravenous administration of fenoterol (in 2013). The aim of our study was to contrast cost and effectiveness of fenoterol therapy in pregnant women at risk of preterm labor during two consecutive years: 2012 - when fenoterol had been widely used (group A), and 2013 when its extensive use had been withdrawn (group B).
3.β Adrenergic Receptor Kinase C-Terminal Peptide Gene-Therapy Improves β2-Adrenergic Receptor-Dependent Neoangiogenesis after Hindlimb Ischemia.
Cannavo A1, Liccardo D1, Lymperopoulos A1, Gambino G1, D'Amico ML1, Rengo F1, Koch WJ1, Leosco D2, Ferrara N1, Rengo G1. J Pharmacol Exp Ther. 2016 Feb;356(2):503-13. doi: 10.1124/jpet.115.228411. Epub 2015 Nov 24.
After hindlimb ischemia (HI), increased catecholamine levels within the ischemic muscle can cause dysregulation of β2-adrenergic receptor (β2AR) signaling, leading to reduced revascularization. Indeed, in vivo β2AR overexpression via gene therapy enhances angiogenesis in a rat model of HI. G protein-coupled receptor kinase 2 (GRK2) is a key regulator of βAR signaling, and β adrenergic receptor kinase C-terminal peptide (βARKct), a peptide inhibitor of GRK2, has been shown to prevent βAR down-regulation and to protect cardiac myocytes and stem cells from ischemic injury through restoration of β2AR protective signaling (i.e., protein kinase B/endothelial nitric oxide synthase). Herein, we tested the potential therapeutic effects of adenoviral-mediated βARKct gene transfer in an experimental model of HI and its effects on βAR signaling and on endothelial cell (EC) function in vitro. Accordingly, in this study, we surgically induced HI in rats by femoral artery resection (FAR).
4.Bone morphogenetic protein receptor type II deficiency and increased inflammatory cytokine production. A gateway to pulmonary arterial hypertension.
Soon E1,2, Crosby A1, Southwood M2, Yang P1, Tajsic T1,3, Toshner M1, Appleby S1, Shanahan CM3, Bloch KD4, Pepke-Zaba J2, Upton P1, Morrell NW1. Am J Respir Crit Care Med. 2015 Oct 1;192(7):859-72. doi: 10.1164/rccm.201408-1509OC.
RATIONALE: Mutations in bone morphogenetic protein receptor type II (BMPR-II) underlie most cases of heritable pulmonary arterial hypertension (PAH). However, disease penetrance is only 20-30%, suggesting a requirement for additional triggers. Inflammation is emerging as a key disease-related factor in PAH, but to date there is no clear mechanism linking BMPR-II deficiency and inflammation.
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CAS 1944-12-3 Fenoterol HBr

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