Tamsulosin hydrochlorideTamsulosin hydrochloride
MedChemExpress (MCE)
HY-B0661A
106463-17-6
(R)-(-)-YM12617
LY253351
99.81%
4°C, sealed storage, away from moisture and light *In solvent : -80°C, 6 months
-20°C, 1 month (sealed storage, away from moisture and light)
Room temperature in continental US
may vary elsewhere.
Tamsulosin hydrochloride ((R)-(-)-YM12617 free base) is an orally active antagonist of α1-adrenergic receptor. Tamsulosin hydrochloride induces Apoptosis. Tamsulosin hydrochloride is used for the research of prostatic hyperplasia. Tamsulosin hydrochloride attenuates abdominal aortic aneurysm growth and inhibits inflammation in animal models.
Tamsulosin hydrochloride shows intrinsic activity at human alpha1B adrenergic receptor expressed in CHOK1 cells co-expressing aequorin, with EC50 of 0.13 nM[2]. Tamsulosin (25-50 nM, 24 h) hydrochloride attenuates high glucose-induced injury in glomerular endothelial cells[3]. Tamsulosin (1-100 μM, 5 days) hydrochloride significantly influences ECM production and distribution as well as cellular metabolism levels in ARPE 19 cells in a concentration-dependent manner[4].. Tamsulosin (50-400 μM, 24 h) hydrochloride induces apoptosis and clusterin expression in NRP-152 cells[5]..
Tamsulosin (0.001-1 mg/kg, gavage, subacutely, 3 doses within 24 h (1, 5 and 23 h) or acutely 60 min before the behavioral tests) hydrochloride facilitates depressive-like behaviors through endogenous glucocorticoids in mice[6]. Tamsulosin (0.01-1 mg/kg, p.o., once a day for 14 consecutive days) hydrochloride exerts inhibitory effect on neuronal activation in the voiding centers of rats with Cyclophosphamide (HY-17420)-induced overactive bladder[7]. Tamsulosin (17.5-35 mcg/kg/d, p.o.) hydrochloride results in protection from respiratory inflammatory events in rats with induced airway sensitization[8].
α1-adrenergic receptor
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19(6):397-404. [Content Brief]
[2]. Rak A, et al. Arylsulfonamide derivatives of (aryloxy)ethyl pyrrolidines and piperidines as α1-adrenergic receptor antagonist with uro-selective activity. Bioorg Med Chem. 2016 Nov 1
24(21):5582-5591. [Content Brief]
[3]. Sun L, et al. Tamsulosin attenuates high glucose- induced injury in glomerular endothelial cells. Bioengineered. 2021 Dec
12(1):5184-5194. [Content Brief]
[4]. Ida Y, et al. The Selective α1 Antagonist Tamsulosin Alters ECM Distributions and Cellular Metabolic Functions of ARPE 19 Cells in a Concentration-Dependent Manner. Bioengineering (Basel). 2022 Oct 14
9(10):556. [Content Brief]
[5]. Youm Y H, et al. Apoptosis Induction and Clusterin Expression of NRP-152 Cells by Tamsulosin. Journal of the Korean Continence Society, 2006, 10(2): 132-139.
[6]. Holanda VAD, et al. Tamsulosin facilitates depressive-like behaviors in mice: Involvement of endogenous glucocorticoids. Brain Res Bull. 2022 Jan
178:29-36. [Content Brief]
[7]. Kim SE, et al. Effects of Tamsulosin on Urinary Bladder Function and Neuronal Activity in the Voiding Centers of Rats with Cyclophosphamide-induced Overactive Bladder. Int Neurourol J. 2012 Mar
16(1):13-22. [Content Brief]
[8]. Alabdali H H, et al. Study the anti-inflammatory effects of tamsulosin by the evaluation of inflammatory cells and lung histopathology in an airway inflammation model in rats. Bulletin of Pharmaceutical Sciences. Assiut, 2023, 46(1): 633-645.