PeptideDB

Fenoterol

CAS: 13392-18-2 F: C17H21NO4 W: 303.35

Fenoterol (Th-1165), a sympathomimetic agent, is a selective and orally active β2-adrenoceptor agonist. Fenoterol is an
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Bioactivity Fenoterol (Th-1165), a sympathomimetic agent, is a selective and orally active β2-adrenoceptor agonist. Fenoterol is an effective bronchodilator and can be used for bronchospasm associated with asthma, bronchitis and other obstructive airway diseases research[1][2].
Invitro Fenoterol (1 μM; pre-incubated 30 minutes) treatment reduces AICAR-induced AMPK activation, NF-κB activation and TNF-α release, and also significantly downregulates the elevated phosphorylation levels of AMPK[2].Fenoterol inhibits lipopolysaccharide (LPS)-induced AMPK activation and inflammatory cytokine production in THP-1 cells[2].Fenoterol is also a potent exosome biogenesis and/or secretion activator in PC cells[4]. Western Blot Analysis[2] Cell Line:
In Vivo Fenoterol (0.7 mg/kg; intraperitoneal injection; twice a day; for 3 weeks) treatment suppresses mechanical allodynia during chronic treatment[3]. Animal Model:
Name Fenoterol
CAS 13392-18-2
Formula C17H21NO4
Molar Mass 303.35
Appearance Solid
Transport Room temperature in continental US; may vary elsewhere.
Storage

4°C, protect from light

*In solvent : -80°C, 6 months; -20°C, 1 month (protect from light)

Reference [1]. R C Heel, et al. Fenoterol: a review of its pharmacological properties and therapeutic efficacy in asthma. Drugs. 1978 Jan;15(1):3-32. [2]. Wei Wang, et al. Anti-inflammatory activities of fenoterol through β-arrestin-2 and inhibition of AMPK and NF-κB activation in AICAR-induced THP-1 cells. Biomed Pharmacother. 2016 Dec;84:185-190. [3]. Nada Choucair-Jaafar, et al. Beta2-adrenoceptor agonists alleviate neuropathic allodynia in mice after chronic treatment. Br J Pharmacol. 2009 Dec;158(7):1683-94. [4]. Amrita Datta, et al. High-throughput screening identified selective inhibitors of exosome biogenesis and secretion: A drug repurposing strategy for advanced cancer. Sci Rep. 2018 May 25;8(1):8161.