research use only
Cat.No.S4740
| Related Targets | Adrenergic Receptor AChR COX Calcium Channel Histamine Receptor Dopamine Receptor GABA Receptor TRP Channel Cholinesterase (ChE) GluR |
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| Other 5-HT Receptor Inhibitors | WAY-100635 Maleate Puerarin Serotonin (5-HT) HCl SB269970 HCl Ketanserin BRL-15572 Dihydrochloride Nuciferine RS-127445 Flopropione Azacyclonol |
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In vitro |
Water : 43 mg/mL
DMSO
: 2 mg/mL
(9.25 mM)
Ethanol : Insoluble |
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In vivo |
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Method for preparing in vivo formulation: Take μL DMSO master liquid, next add μL Corn oil, mix and clarify.
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| Molecular Weight | 216.17 | Formula | C10H9O4.Na |
Storage (From the date of receipt) | |
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| CAS No. | 24276-84-4 | Download SDF | Storage of Stock Solutions |
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| Synonyms | Ferulic acid sodium salt | Smiles | COC1=C(C=CC(=C1)C=CC(=O)[O-])O.[Na+] | ||
| In vitro |
SF is stable, water soluble. In vitro, SF (0.4 mg/mL) inhibits platelet aggregation induced by adenosine diphosphate (ADP) or collagen. At 1 mg/mL SF inhibits thrombin-induced platelet aggregation and release of [3H]5-HT from labelled platelets. The mechanism of SF action appears to be mediated by inhibition of cyclooxygenase and TXA2 synthase. In vitro SF inhibits lipid peroxide malondialdehyde (MDA) production from the platelets of rats, inhibits haemolysis induced by MDA and hydroxyl radical (OH·), and in erythrocyte membranes it inhibits lipid peroxidation induced by hydrogen peroxide (H2O2) and superoxide anions (O2-). SF is a direct scavenger of oxygen free radicals. SF is found to act as a novel non-peptide endothelin antagonist and to prevent the binding of ET-1 to its receptor.
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| In vivo |
SF has antithrombotic, platelet aggregation inhibitory and antioxidant activities in animals and humans. In ethanol, carbon tetrachloride-, paracetamol-, or prednisolone-induced liver toxicity in mice, SF, 0.1 g/kg intragastrically, daily for 10 days inhibits the rise of liver lipid peroxides MDA content and alleviates liver lesions by stabilizing glutathione (GSH) and related enzymes levels. In glycerol-induced renal oxidative injury in mice, SF at 0.2 g/kg i.p., reverses the increase of renal MDA content and the decrease of GSH content, glutathione peroxidase (GSH-Px), glutathione S-transferase (GST), catalase (Cat), and SOD activities induced by glycerol injection, and improves renal histology. SF has a clear protective effect in experimental myocardial ischemia. In rabbits SF reduces the area of experimental myocardial infarction by 41% and decreases the oxygen consumption of guinea pig myocardial homogenates. SF has also a protective effect in myocardial ischemia reperfusion injury of rats. Furthermore, SF has an anti-atherogenetic effect in animal models. The antiarrhythmic effects of SF have been demonstrated in experimental animal models of arrhythmia, but not yet in clinical studies. The elimination half-life of SF is about 9.86 min. The acute oral LD50 of SF in mice is 3.2 g/kg.
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References |
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