Betaxolol hydrochloride
Chemical Name: 1-[4-[2-(Cyclopropylmethoxy)ethyl]phenoxy]-3-isopropylamino-2-propanol hydrochloride
Purity: ≥99%
Biological Activity
Betaxolol hydrochloride is a selective β1-adrenoceptor antagonist.Technical Data
The technical data provided above is for guidance only.
For batch specific data refer to the Certificate of Analysis.
Tocris products are intended for laboratory research use only, unless stated otherwise.
Background References
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High-throughput genotoxicity assay identifies antioxidants as inducers of DNA damage response and cell death.
Fox JT, Sakamuru S, Huang R
Proc. Natl. Acad. Sci. U.S.A., 2012;109(14):5423-8. -
Betaxolol. A review of its pharmacodynamic and pharmacokinetic properties and therapeutic efficacy in hypertension.
Beresford and Heel
Drugs, 1986;31:6 -
The affinity of betaxolol, a β1-adrenoceptor-selective blocking agent, for β-adrenoceptors in the bovine trachea and heart
Satoh et al.
Br.J.Pharmacol., 1993;108:484 -
Inhibitory action of betaxolol, a β1-selective adrenoceptor antagonist, on voltage-dependent calcium channels in guinea pig artery and vein.
Setoguchi et al.
Br.J.Pharmacol., 1995;115:198
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Citations for Betaxolol hydrochloride
The citations listed below are publications that use Tocris products. Selected citations for Betaxolol hydrochloride include:
5 Citations: Showing 1 - 5
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Recruitment of β-arrestin 1 and 2 to the β2-adrenoceptor: analysis of 65 ligands.
Authors: Littmann Et al.
Cardiovasc Res 2015;355:183
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β-Adrenergic receptors enhance excitatory transmission in the bed nucleus of the stria terminalis through a corticotrophin-releasing factor receptor-dependent and cocaine-regulated mechanism.
Authors: Nobis Et al.
Biol Psychiatry 2011;69:1083
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Stress and glucocorticoids impair memory retrieval via β2-adrenergic, Gi/o-coupled suppression of cAMP signaling.
Authors: Schutsky Et al.
J Neurosci 2011;31:14172
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β1-Adrenergic receptors activate two distinct signaling pathways in striatal neurons.
Authors: Meitzen Et al.
J Neurochem 2011;116:984
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Catechol-O-methyltransferase inhibition increases pain sensitivity through activation of both beta2- and beta3-adrenergic receptors.
Authors: Nackley Et al.
Pain 2007;128:199
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