product name Fluoxetine HCl
Description: Fluoxetine HCl (also known as Lilly110140), the HCl salt of fluoxetine, is a selective serotonin-reuptake inhibitor (SSRI) at the neuronal membrane, it is used in the treatment of depression. It is also used for the treatment of obsessive–compulsive disorder, bulimia nervosa, panic disorder, and premenstrual dysphoric disorder. Fluoxetine may decrease the risk of suicide in those over the age of 65. Fluoxetine has also been used to treat premature ejaculation. It is taken by mouth.
References: Neuropsychopharmacology. 2003 Sep;28(9):1562-71; Neuropsychopharmacology. 2000 Sep;23(3):250-62.
345.79
Formula
C17H18F3NO.HCl
CAS No.
56296-78-7
Storage
-20℃ for 3 years in powder form
-80℃ for 2 years in solvent
Solubility (In vitro)
DMSO: 69 mg/mL (199.5 mM)
Water: <1 mg/mL
Ethanol: 69 mg/mL (199.5 mM)
Solubility (In vivo)
Synonyms
Lilly110140
other peoduct :
| In Vitro |
In vitro activity: Fluoxetine blocks the downregulation of cell proliferation resulting from inescapable shock (IS) of hippocampal cell. Fluoxetine increases the number of newborn cells in the dentate gyrus of the hippocampus of adult rat. Fluoxetine also increases the number of proliferating cells in the prelimbic cortex. Fluoxetine accelerates the maturation of immature neurons. Fluoxetine enhances neurogenesis-dependent long-term potentiation (LTP) in the dentate gyrus. Fluoxetine, but not citalopram, fluvoxamine, paroxetine and sertraline, increases norepinephrine and dopamine extracellular levels in prefrontal cortex. Fluoxetine produces robust and sustained increases in extracellular concentrations of norepinephrine and dopamine after acute systemic administration. Kinase Assay: Cell Assay: In Xenopusoocytes expressing either cloned 5HT2C receptors or 5HT receptors, micromolar concentrations of fluoxetine (Prozac) inhibited the membrane currents elicited by serotonin (5-hydroxytryptamine; 5HT). For responses elicited by 1 μM 5-HT, the IC50 of fluoxetine was about 20 μM. Fluoxetine also inhibited the binding of [3H]5HT to 5HT2C receptors expressed in HeLa cells and the binding of [3H]5HT to 5HT receptors in rat cortex membranes, with Ki of ≈65–97 nM and ≈ 56 μM, respectively. Administration of fluoxetine blocked the downregulation of cell proliferation of hippocampal cells resulting from inescapable shock (IS), which resulted in a state of behavioral despair. Fluoxetine increased the number of newborn cells in the dentate gyrus of the hippocampus of adult rat. Fluoxetine also increased the number of proliferating cells in the prelimbic cortex. Fluoxetine accelerated the maturation of immature neurons. Fluoxetine enhanced neurogenesis-dependent long-term potentiation (LTP) in the dentate gyrus. Fluoxetine, but not other selective serotonin uptake inhibitors such as citalopram, fluvoxamine, paroxetine and sertraline, increased norepinephrine and dopamine extracellular levels in prefrontal cortex. Fluoxetine produced robust and sustained increases in extracellular concentrations of norepinephrine and dopamine after acute systemic administration. |
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| In Vivo | Fluoxetine treatment also reverses the deficit in escape latency observed in animals exposed to inescapable shock in adult male Sprague–Dawley rats. Fluoxetine combined with Olanzapine produces robust, sustained increases of extracellular levels of dopamine ([DA](ex)) and norepinephrine ([NE](ex)) up to 361% and 272% of the baseline, respectively, which are significantly greater than either drug alone. |
| Animal model | |
| Formulation & Dosage | |
| References | Neuropsychopharmacology. 2003 Sep;28(9):1562-71; Neuropsychopharmacology. 2000 Sep;23(3):250-62. |
