Paroxetine hydrochloride hemihydrate (BRL29060 hydrochloride hemihydrate) |
| カタログ番号GC30992 |
パロキセチン塩酸塩半水和物 (BRL29060 塩酸塩半水和物) は、強力な選択的セロトニン再取り込み阻害剤であり、一般に抗うつ薬として処方され、IC50 が 14μ の GRK2 阻害能を持っています。
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Cas No.: 110429-35-1
Sample solution is provided at 25 µL, 10mM.
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Paroxetine hydrochloride hemihydrate is a potent selective serotonin-reuptake inhibitor, commonly prescribed as an antidepressant and has GRK2 inhibitory ability with IC50 of 14 μM.
Paroxetine (1 μM and 10 μM) distinctly restrains T cell migration induced by CX3CL1 through inhibiting GRK2. Paroxetine inhibits GRK2 induced activation of ERK[1]. Paroxetine (10 μM) reduces pro-inflammatory cytokines in LPS-stimulated BV2 cells. Paroxetine (0-5 μM) leads to a dose-dependent inhibition on LPS-induced production of TNF-α and IL-1β in BV2 cells. Paroxetine also inhibits lipopolysaccharide (LPS)-induced nitric oxide (NO) production and inducible nitric oxide synthase (iNOS) expression in BV2 cells. Paroxetine (5 μM) blocks LPS-induced JNK activation and attenuates baseline ERK1/2 activity in BV2 cells. Paroxetine relieves microglia-mediated neurotoxicity, and suppresses LPS-stimulated pro-inflammatory cytokines and NO in primary microglial cells[4].
Paroxetine treatment obviously attenuates the symptoms of CIA rats. Paroxetine treatment clearly prevents the histological damage of joints and alleviates T cells infiltration into synovial tissue. Paroxetine reveals a strong effect on inhibiting CX3CL1 production in synovial tissues[1]. Paroxetine (20 mg/kg/day) reduces the myocyte cross-sectional area in rat and ROS formation in the remote myocardium. Paroxetine reduces the susceptibility to ventricular tachycardia. Paroxetine treatment following MI decreases LV remodeling and susceptibility to arrhythmias, probably by reducing ROS formation[2]. In CCI paroxetine-treated group, paroxetine (10 mg/kg, i.p.) produces hyperalgesia at days 7 and 10 (P<0.01), but a decrease in pain behavior is seen at day 14. Moreover, paroxetine (10 mg/kg) significantly attenuates tactile hypersensitivity when compared to CCI vehicle-treated group[5].
[1]. Wang Q, et al. Paroxetine alleviates T lymphocyte activation and infiltration to joints of collagen-induced arthritis. Sci Rep. 2017 Mar 28;7:45364. [2]. Lassen TR, et al. Effect of paroxetine on left ventricular remodeling in an in vivo rat model of myocardial infarction. Basic Res Cardiol. 2017 May;112(3):26. [3]. Waldschmidt HV, et al. Structure-Based Design of Highly Selective and Potent G Protein-Coupled Receptor Kinase 2 Inhibitors Based on Paroxetine. J Med Chem. 2017 Apr 13;60(7):3052-3069. [4]. Liu RP, et al. Paroxetine ameliorates lipopolysaccharide-induced microglia activation via differential regulation of MAPK signaling. J Neuroinflammation. 2014 Mar 12;11:47.
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