2. Metabolic Enzyme/Protease Neuronal Signaling GPCR/G Protein Immunology/Inflammation
  3. Cytochrome P450 5-HT Receptor NO Synthase
  4. Paroxetine acetate

Paroxetine (BRL29060) acetate is a selective serotonin reuptake inhibitor with blood-brain barrier permeability. Paroxetine acetate inhibits nitric oxide synthase and CYP2D6, induces desensitization of 5-HT1A/1B/1D autoreceptors, downregulates 5-HT2 receptors, and promotes the production of inflammatory cytokines. Paroxetine acetate is widely used in the research of related diseases such as depression, obsessive-compulsive disorder, panic disorder, social phobia, generalized anxiety disorder, post-traumatic stress disorder, premenstrual dysphoric disorder and hot flashes.

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CAS No. : 72471-80-8

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Paroxetine acetate Related Antibodies

Top Publications Citing Use of Products

    Paroxetine acetate purchased from MedChemExpress. Usage Cited in: Drug Des Devel Ther. 2026 Jan 27;20:1-16.

    CCK-8 assay was performed with different concentrations of Paroxetine (0.0625-10 μM) in BMMs for 1 day and 3 days.

    Paroxetine acetate purchased from MedChemExpress. Usage Cited in: Drug Des Devel Ther. 2026 Jan 27;20:1-16.

    Assessment of mRNA expression levels of osteoclastogenesis-associated marker genes after administration with Paroxetine (0.0625-2.5 μM) by RT-qPCR, including NFATc1, c-fos, RANK, TRAP, Cathepsin K, and MMP9. he results showed that Paroxetine inhibited the expression of NFATc1, c-fos, RANK, TRAP, Cathepsin K, and MMP9 genes in a concentration-dependent manner.

    Paroxetine acetate purchased from MedChemExpress. Usage Cited in: Drug Des Devel Ther. 2026 Jan 27;20:1-16.

    Assessment of protein expression levels of NFATc1, c-fos, Cathepsin K and MMP9 after administration with Paroxetine (0.0625-2.5 μM; pretreatment 2 h before stimulation+ 3 d after stimulation) by Western blot. The results demonstrated that, following RANKL stimulation, the protein expression levels of NFATc1, c-fos, CTSK, and MMP9 significantly increased. However, Paroxetine reduced the expression levels of these proteins in osteoclasts in a concentration-dependent manner.

    Paroxetine acetate purchased from MedChemExpress. Usage Cited in: Drug Des Devel Ther. 2026 Jan 27;20:1-16.

    Representative fluorescence images of P65 nuclear translocation following RANKL stimulation without or with Paroxetine (PA) (pretreatment 6 h). The results showed that RANKL stimulation led to a significant increase in the mean nuclear fluorescence intensity of p65, whereas Paroxetine treatment attenuated this effect.

    Paroxetine acetate purchased from MedChemExpress. Usage Cited in: Drug Des Devel Ther. 2026 Jan 27;20:1-16.

    Histopathology photographs of femoral samples after HE-stained sections. The results revealed that the trabecular bone in the distal femoral region of mice in the LPS group became sparse and thin. In contrast, Paroxetine (PA, 20 mg/kg; i.p.; once daily for 10 days) effectively alleviated bone loss, as evidenced by the intact and well-ordered arrangement of trabeculae in mice of this group.

    Paroxetine acetate purchased from MedChemExpress. Usage Cited in: Drug Des Devel Ther. 2026 Jan 27;20:1-16.

    Representative TRAP staining images of RANKL-induced osteoclasts treated with Paroxetine (2.5 μM) on specified days. The results showed that the addition of Paroxetine during the early stage of differentiation (days 1-3) significantly inhibited osteoclast formation. In contrast, when bone marrow-derived macrophages (BMMs) were exposed to Paroxetine from days 3-5 or days 5-7, the number of osteoclasts was also reduced, but the inhibitory effect was less pronounced compared to the early-stage (days 1–3) exposure.

    Paroxetine acetate purchased from MedChemExpress. Usage Cited in: NPJ Digit Med. 2025 Nov 17;8(1):663.  [Abstract]

    Heat map display of cell viabilities of A549 (Left) and H1299 (Right) cells after incubation with different concentrations of anti-ED compounds (Paroxetine (10–200 μg/mL), et al.) for 48 h. The results showed that paroxetine did not significantly promote tumor cell proliferation; instead, it exerted a mild inhibitory effect on cell growth at higher concentrations.

    Paroxetine acetate purchased from MedChemExpress. Usage Cited in: Cell Rep. 2025 Apr 2;44(4):115489.  [Abstract]

    Paroxetine (5 mg/kg; i.p.; once daily for 2–3 weeks) alleviated pain and depression-like symptoms in mice subjected to chronic restraint stress (CRS).

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    nNOS iNOS eNOS

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    Description

    Paroxetine (BRL29060) acetate is a selective serotonin reuptake inhibitor with blood-brain barrier permeability. Paroxetine acetate inhibits nitric oxide synthase and CYP2D6, induces desensitization of 5-HT1A/1B/1D autoreceptors, downregulates 5-HT2 receptors, and promotes the production of inflammatory cytokines. Paroxetine acetate is widely used in the research of related diseases such as depression, obsessive-compulsive disorder, panic disorder, social phobia, generalized anxiety disorder, post-traumatic stress disorder, premenstrual dysphoric disorder and hot flashes[1][2][3].

    IC50 & Target[1]

    CYP2D6

     

    5-HT2 Receptor

     

    In Vitro

    Paroxetine potently and selectively inhibits serotonin reuptake in rat brain synaptosomes, with a Ki of 1.1 nmol/L, and shows much weaker activity against norepinephrine and dopamine reuptake[1].
    Paroxetine has no significant affinity for most tested neurotransmitter receptors in rat brain tissue, only showing weak binding to muscarinic cholinergic receptors with a Ki of 89 nmol/L[1].
    Paroxetine (76 nM) exhibits high affinity for the muscarinic M1 receptor, resulting in greater anticholinergic effects than other SSRIs[2].
    Paroxetine exhibits estrogenic activity in an in vitro assay that identifies chemicals disrupting aromatase and estrogen balance in humans, which may promote estrogen-sensitive breast tumor growth[2].
    Paroxetine (10-20 μM; 6-24 h) differentially modulates LPS-induced cytokine production in Raw264.7 mouse macrophages, potently inhibiting IL-6 production and enhancing TNFα production at 10 μM and 20 μM concentrations after 6 and 24 hours of incubation[3].
    Paroxetine (10-20 μM; 6-24 h) differentially modulates LPS-induced cytokine production in thioglycollate-elicited primary mouse peritoneal macrophages, potently inhibiting IL-6 production and enhancing TNFα production at 10 μM and 20 μM concentrations after 6 and 24 hours of incubation[3].
    Paroxetine (20 μM; 24 h) inhibits LPS-induced IL-6 production independent of 5-HT2/5-HT7 receptors and enhances LPS-induced TNFα production via 5-HT2/5-HT7 receptors in Raw264.7 mouse macrophages after 24 hours of incubation[3].
    Paroxetine (20 μM) modulates LPS-induced IL-6 and TNFα production in Raw264.7 mouse macrophages independently of GRK2, as its inhibitory effect on IL-6 and enhancing effect on TNFα are retained in GRK2-knockdown cells[3].

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

    Paroxetine acetate Related Antibodies

    ELISA Assay[3]

    Cell Line: Raw264.7 mouse macrophages
    Concentration: 10 μM; 20 μM
    Incubation Time: 6 h; 24 h
    Result: Reduced LPS-induced IL-6 production to ~75% of LPS-only levels at 6 hours with 10 μM.
    Reduced LPS-induced IL-6 production to ~50% of LPS-only levels at 6 hours with 20 μM.
    Reduced LPS-induced IL-6 production to ~80% of LPS-only levels at 24 hours with 10 μM.
    Reduced LPS-induced IL-6 production to ~60% of LPS-only levels at 24 hours with 20 μM.
    Increased LPS-induced TNFα production to ~155% of LPS-only levels at 6 hours with 10 μM.
    Increased LPS-induced TNFα production to ~195% of LPS-only levels at 6 hours with 20 μM.
    Increased LPS-induced TNFα production to ~120% of LPS-only levels at 24 hours with 10 μM.
    Increased LPS-induced TNFα production to ~145% of LPS-only levels at 24 hours with 20 μM.

    ELISA Assay[3]

    Cell Line: Raw264.7 mouse macrophages pretreated with 5-HT2/5-HT7 receptor antagonist LY215840
    Concentration: 20 μM
    Incubation Time: 24 h
    Result: Reduced LPS-induced IL-6 production to ~45% of LPS-only levels.
    Increased LPS-induced TNFα production to ~180% of LPS-only levels.
    Co-treatment with LY215840 (10 nM, 100 nM, 1 μM) further reduced IL-6 levels to below ~20% of LPS-only levels.
    Co-treatment with LY215840 (10 nM, 100 nM, 1 μM) reversed TNFα enhancement, reducing levels to ~80%, ~40%, and ~40% of LPS-only levels, respectively (for 100 nM and 1 μM LY215840).
    In Vivo

    Paroxetine (8–32 mg/kg) acetate produces a dose-dependent anti-immobility effect in the mouse forced swim test and also exhibits noradrenergic activity[1].
    Paroxetine acetate exerts no significant dopaminergic, sedative, or ethanol-potentiating effects in healthy rodent models[1].
    Paroxetine acetate produces extremely mild cardiovascular effects in healthy cats, rabbits, and dogs compared with tricyclic antidepressants, and exhibits weak quinidine-like activity only at serotonin reuptake-blocking doses[1].
    Combination of Paroxetine acetate with monoamine oxidase inhibitors (MAOIs) or serotonin precursors induces serotonin syndrome in rats[1].
    Paroxetine acetate modulates the hypothalamic-pituitary-adrenal axis and prolactin-related endocrine activity in healthy rats[1].
    Acute treatment with paroxetine acetate (5 mg/kg) increases extracellular serotonin levels in the brain of healthy rats[1].
    Paroxetine acetate antagonizes apomorphine-induced hypothermia in rats, indicating that it exhibits noradrenergic activity at high doses[1].
    Combination treatment with paroxetine acetate (for 3 consecutive weeks) and pravastatin increases the blood glucose level of prediabetic, insulin-resistant mice from 128 mg/dl to 193 mg/dl[2].

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

    Animal Model: Mouse forced swimming test[1]
    Dosage: 8, 16, 32 mg/kg
    Administration: /
    Result: Produced a dose-dependent anti-immobility effect in the mouse forced swimming test.
    Exhibited serotonergic activity at low doses (8, 16 mg/kg), while it displays both serotonergic and noradrenergic activities at the high dose of 32 mg/kg.
    Molecular Weight

    389.42

    Formula

    C21H24FNO5
    CAS No.
    SMILES

    C(C)(O)=O.C(OC=1C=C2C(=CC1)OCO2)[C@H]3[C@@H](CCNC3)C4=CC=C(F)C=C4
    Shipping

    Room temperature in continental US; may vary elsewhere.
    Storage

    Please store the product under the recommended conditions in the Certificate of Analysis.
    Purity & Documentation
    References
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    Paroxetine acetate Related Classifications

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    • Do most proteins show cross-species activity?

      Species cross-reactivity must be investigated individually for each product. Many human cytokines will produce a nice response in mouse cell lines, and many mouse proteins will show activity on human cells. Other proteins may have a lower specific activity when used in the opposite species.

    Keywords:

    Paroxetine72471-80-8BRL29060BRL 29060BRL-29060Cytochrome P4505-HT ReceptorNO SynthaseCYPsSerotonin Receptor5-hydroxytryptamine ReceptorNitric oxide synthasesNOS5-HT2 receptorsRaw264.7 mouse macrophagesnitric oxide synthase5-HT1B/1D autoreceptorsserotonin reuptake transportercytochrome P450 3A45-HT1A autoreceptornorepinephrine reuptake transportercytochrome P450 2D6muscarinic cholinergic receptorInhibitorinhibitorinhibit

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