1. Neuronal Signaling
    Autophagy
  2. Serotonin Transporter
    Autophagy
  3. Paroxetine hydrochloride hemihydrate

Paroxetine hydrochloride hemihydrate (Synonyms: BRL29060 hydrochloride hemihydrate; BRL29060A hemihydrate)

Cat. No.: HY-B0492A
Handling Instructions

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.

For research use only. We do not sell to patients.

Paroxetine hydrochloride hemihydrate Chemical Structure

Paroxetine hydrochloride hemihydrate Chemical Structure

CAS No. : 110429-35-1

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Top Publications Citing Use of Products

Publications Citing Use of MCE Paroxetine hydrochloride hemihydrate

    Paroxetine hydrochloride hemihydrate purchased from MCE. Usage Cited in: Brain Res. 2019 Oct 1;1720:146296.

    Protein levels of IFNα and IRF2(B) are detected in HA1800 Cells at 6 h, 12 h and 24 h after paroxetine (10μM) treatment by RT-qPCR and western blot respectively.
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    Description

    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.

    IC50 & Target

    IC50: 14 μM (GRK2)[3]

    In Vitro

    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].

    MCE has not independently confirmed the accuracy of these methods. They are for reference only.

    In Vivo

    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].

    MCE has not independently confirmed the accuracy of these methods. They are for reference only.

    Clinical Trial
    Molecular Weight

    374.83

    Formula

    C₁₉H₂₀FNO₃.Cl H.₁/₂H₂O

    CAS No.
    SMILES

    FC1=CC=C([[email protected]@H]2[[email protected]@H](COC3=CC=C4OCOC4=C3)CNCC2)C=C1.[0.5H2O].Cl

    Shipping

    Room temperature in continental US; may vary elsewhere.

    Storage

    Please store the product under the recommended conditions in the Certificate of Analysis.

    References
    Cell Assay
    [4]

    Cell viability is determined by the tetrazolium salt 3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyltetrazolium bromide (MTT) assay. BV2 and primary microglial cells are initially seeded into 96-well plates at a density of 1×104 cells/well and 5×104 cells/well, respectively. Following treatment, MTT (5 mg/mL in PBS) is added to each well and incubated at 37°C for four hours. The resulting formazan crystals are dissolved in dimethylsulfoxide (DMSO). The optical density is measured at 570 nm, and results are expressed as a percentage of surviving cells compared with the control.

    MCE has not independently confirmed the accuracy of these methods. They are for reference only.

    Animal Administration
    [5]

    Animals are divided into two main groups: 1) pre-emptive and 2) post-injury group. Each main group is divided into three different subgroups: I) CCI vehicle-treated group, II) sham group, and III) CCI paroxetine-treated group. Vehicle is injected i.p. to CCI and sham-operated animals. In the pre-emptive study, paroxetine (10 mg/kg) is injected 1 h before surgery and continued daily until day 14 post surgery. In the post-injury group, paroxetine (10 mg/kg) is administered at day 7 post injury and continued daily until day 14. All behavioral tests are recorded on day 0 (control day) before surgery and on days 1, 3, 5, 7, 10, and 14 post-nerve injury.

    MCE has not independently confirmed the accuracy of these methods. They are for reference only.

    References
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    Keywords:

    Paroxetine hydrochloride hemihydrateBRL29060 hydrochloride hemihydrate BRL29060A hemihydrateSerotonin TransporterAutophagy5-HTTSERTSLC6A4Inhibitorinhibitorinhibit

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