110429-35-1
基本信息
D4-盐酸帕罗西汀
盐酸帕罗西汀半水合物
盐酸帕罗西汀半水合物, 选择性5-羟色胺重吸收抑制剂 (SSRI)
(办证)盐酸帕罗西汀PAROXETINE HYDROCHLORIDE HEMIHYDRAT
(-)-(3S,4R)-PAROXETINE HYDROCHLORIDE HEMIHYDRATE
(-)-反式-4R-(4-氟苯基)-3S-{[3',4'-(亚甲二氧基)苯氧基]甲基}-哌啶盐酸盐半水合物
BRL29060A hemihydrate
PAROXETINE HCL HEMIHYDRATE
Paroxetine-D4 hydrochloride
PAROXETINE-D4 HCL USP/EP/BP
PAROXETINE HYDROCHLORIDE 1/2H2O
paroxetine hydrochloride hydrate
Paroxetine Hydrochloride (350 mg)
PAROXETINE HEMIHYDRATE, EP/BP/USP
BRL29060 hydrochloride hemihydrate
物理化学性质
| 熔点 | 121-131 C |
| 储存条件 | Inert atmosphere,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 | 粉末 |
| 颜色 | 白色 |
| 最大波长(λmax) | 292nm(H2O)(lit.) |
| Merck | 14,7043 |
| CAS 数据库 | 110429-35-1 |
安全数据
| 危险性符号(GHS) |   GHS07,GHS09 |
| 警示词 | 警告 |
| 危险性描述 | H302-H317-H319-H411 |
| 防范说明 | P261-P273-P280-P301+P312-P302+P352-P305+P351+P338 |
| 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 |
盐酸帕罗西汀价格(试剂级)
| 报价日期 | 产品编号 | 产品名称 | CAS号 | 包装 | 价格 |
| 2024/11/08 | 46263 | 盐酸帕罗西汀半水合物 Paroxetine hydrochloride hemihydrate, 98% | 110429-35-1 | 1g | 602元 |
| 2024/11/08 | 46263 | 盐酸帕罗西汀半水合物 Paroxetine hydrochloride hemihydrate, 98% | 110429-35-1 | 5g | 2055元 |
| 2024/11/08 | P1977 | 盐酸帕罗西汀 半水合物 Paroxetine Hydrochloride Hemihydrate | 110429-35-1 | 1g | 70元 |
常见问题列表
IC50: 14 μM (GRK2)
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.
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.