rel-Paroxetine-d4 hydrochloriderel-Paroxetine-d4 hydrochloride
MedChemExpress (MCE)
HY-151216S
1217683-35-6
rel-BRL29060-d4 hydrochloride
rel-BRL29060A-d4
Please store the product under the recommended conditions in the Certificate of Analysis.
Room temperature in continental US
may vary elsewhere.
rel-Paroxetine-d4 (hydrochloride) is an isotope-labeled Paroxetine hydrochloride (HY-B0492). Paroxetine hydrochloride is an orally active and selective serotonin-reuptake inhibitor, commonly prescribed as an GRK2 inhibitor with IC50 of 14 μM. Paroxetine hydrochloride can be used for the research of depressive disorder[1][2][3][4].
Stable heavy isotopes of hydrogen, carbon, and other elements have been incorporated into drug molecules, largely as tracers for quantitation during the drug development process. Deuteration has gained attention because of its potential to affect the pharmacokinetic and metabolic profiles of drugs[1]. Paroxetine (1 μM and 10 μM
4 h) distinctly restrains T cell migration induced by CX3CL1 through inhibiting GRK2[2]. Paroxetine (16 h) inhibits GRK2 induced activation of ERK in splenic T cells[2]. Paroxetine (10 μM) reduces pro-inflammatory cytokines in LPS-stimulated BV2 cells[3]. Paroxetine (0-5 μM) leads to a dose-dependent inhibition on LPS-induced production of TNF-α and IL-1β in BV2 cells[3]. Paroxetine also inhibits lipopolysaccharide (LPS)-induced nitric oxide (NO) production and inducible nitric oxide synthase (iNOS) expression in BV2 cells[3]. Paroxetine (5 μM) blocks LPS-induced JNK activation and attenuates baseline ERK1/2 activity in BV2 cells[3]. Paroxetine relieves microglia-mediated neurotoxicity, and suppresses LPS-stimulated pro-inflammatory cytokines and NO in primary microglial cells[3].
Paroxetine (15 mg/kg/d
p.o.
15 d) obviously attenuates the symptoms of collagen-induced arthritis (CIA) rats[2].
IC50: 14 μM (GRK2)[2]
Serotonin-reuptake[4] In Vitro Stable heavy isotopes of hydrogen, carbon, and other elements have been incorporated into drug molecules, largely as tracers for quantitation during the drug development process. Deuteration has gained attention because of its potential to affect the pharmacokinetic and metabolic profiles of drugs[1]. Paroxetine (1 μM and 10 μM
4 h) distinctly restrains T cell migration induced by CX3CL1 through inhibiting GRK2[2]. Paroxetine (16 h) inhibits GRK2 induced activation of ERK in splenic T cells[2]. Paroxetine (10 μM) reduces pro-inflammatory cytokines in LPS-stimulated BV2 cells[3]. Paroxetine (0-5 μM) leads to a dose-dependent inhibition on LPS-induced production of TNF-α and IL-1β in BV2 cells[3]. Paroxetine also inhibits lipopolysaccharide (LPS)-induced nitric oxide (NO) production and inducible nitric oxide synthase (iNOS) expression in BV2 cells[3]. Paroxetine (5 μM) blocks LPS-induced JNK activation and attenuates baseline ERK1/2 activity in BV2 cells[3]. Paroxetine relieves microglia-mediated neurotoxicity, and suppresses LPS-stimulated pro-inflammatory cytokines and NO in primary microglial cells[3]. MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. 0 --> rel-Paroxetine-d4 hydrochloride Related Antibodies
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[1]. Russak EM, et al. Impact of Deuterium Substitution on the Pharmacokinetics of Pharmaceuticals. Ann Pharmacother. 2019
53(2):211-223. [Content Brief]
[2]. Wang Q, et al. Paroxetine alleviates T lymphocyte activation and infiltration to joints of collagen-induced arthritis. Sci Rep. 2017 Mar 28
7:45364. [Content Brief]
[3]. Liu RP, et al. Paroxetine ameliorates lipopolysaccharide-induced microglia activation via differential regulation of MAPK signaling. J Neuroinflammation. 2014 Mar 12
11:47. [Content Brief]
[4]. Hwang S, et al. Inhibitory effect of the selective serotonin reuptake inhibitor paroxetine on human Kv1.3 channels. Eur J Pharmacol. 2021 Dec 5
912:174567. [Content Brief]
