Paroxetine hydrochloride hydrate

Modify Date: 2024-01-02 17:44:30

Paroxetine hydrochloride hydrate Structure
Paroxetine hydrochloride hydrate structure
Common Name Paroxetine hydrochloride hydrate
CAS Number 110429-35-1 Molecular Weight 374.83
Density 1.213g/cm3 Boiling Point 451.7ºC at 760mmHg
Molecular Formula C19H22ClFNO3.5 Melting Point 121-131ºC
MSDS Chinese USA Flash Point 227ºC
Symbol GHS07
GHS07
Signal Word Warning

 Use of Paroxetine hydrochloride hydrate


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.

 Names

Name Paroxetine hydrochloride hemihydrate
Synonym More Synonyms

 Paroxetine hydrochloride hydrate Biological Activity

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.
Related Catalog
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].
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].
Cell Assay 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.
Animal Admin 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.
References

[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.

 Chemical & Physical Properties

Density 1.213g/cm3
Boiling Point 451.7ºC at 760mmHg
Melting Point 121-131ºC
Molecular Formula C19H22ClFNO3.5
Molecular Weight 374.83
Flash Point 227ºC
PSA 39.72000
LogP 4.45730
Appearance of Characters white
Water Solubility Slightly soluble in water, freely soluble in methanol, sparingly soluble in ethanol (96 per cent) and in methylene chloride.

 Safety Information

Symbol GHS07
GHS07
Signal Word Warning
Hazard Statements H302-H315-H319-H335
Precautionary Statements P301 + P312 + P330-P305 + P351 + P338
Personal Protective Equipment dust mask type N95 (US);Eyeshields;Gloves
Hazard Codes F,C
Risk Phrases 11-34-36/37/38-22
Safety Phrases 16-26-36/37/39-45-36
RIDADR 3077.0
RTECS TM4569320
HS Code 2934999090

 Synthetic Route

 Customs

HS Code 2934999090
Summary 2934999090. other heterocyclic compounds. VAT:17.0%. Tax rebate rate:13.0%. . MFN tariff:6.5%. General tariff:20.0%

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 Synonyms

paroxetine hydrochloride ;(-)trans-3-[(1,3-benzodioxol-5-yloxy) methyl]-4-(4-fluorophenyl) paroxetine hydrochloride
(3S,4R)-3-[(1,3-Benzodioxol-5-yloxy)methyl]-4-(4-fluorophenyl)piperidine hydrochloride hydrate (2:2:1)
Piperidine, 3-[(1,3-benzodioxol-5-yloxy)methyl]-4-(4-fluorophenyl)-, (3S,4R)-, hydrochloride, hydrate (2:2:1)
Paroxetine Hydrochloride HeMihydrate
Paroxetine hydrochl
Paroxetine hydrochloride
Paroxetine hydrochloride hydrate
Paroxetine (hydrochloride hemihydrate)