盐酸帕罗西汀

生物活性靶点体外研究体内研究盐酸帕罗西汀试剂级价格

盐酸帕罗西汀

CAS号:110429-35-1
英文名:PAROXETINE-D4 HCL
中文名:盐酸帕罗西汀
CBNumber:CB1178023
分子式:C19H23ClFNO4
分子量:383.84
MOL File:110429-35-1.mol

盐酸帕罗西汀化学性质

熔点 :121-131 C
储存条件 :under inert gas (nitrogen or Argon) at 2-8°C
溶解度 :Slightly soluble in water, freely soluble in methanol, sparingly soluble in ethanol (96 per cent) and in methylene chloride.
形态 :powder
颜色 :white
最大波长(λmax) :292nm(H2O)(lit.)
Merck :14,7043
CAS 数据库 :110429-35-1

安全信息

危险品标志 :F,C,Xn
危险类别码 :11-34-36/37/38-22
安全说明 :16-26-36/37/39-45-36
危险品运输编号 :UN 3077 9 / PGIII
WGK Germany :3
RTECS号 :TM4569320
危险等级 :IRRITANT
海关编码 :29349990

盐酸帕罗西汀性质、用途与生产工艺

生物活性 Paroxetine hydrochloride hemihydrate 是一种抗抑郁药，为高效的五羟色胺再摄取抑制剂，能抑制 GRK2 活性，IC50 值为 14 μM。
靶点

IC50: 14 μM (GRK2)
体外研究

Paroxetine (1 μM and 10 μM) distinctly restrains T cell migration induced by CX3CL1 through inhibiting GRK2. Paroxetine inhibits GRK2 induced activation of ERK. 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.
体内研究

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. 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. 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.