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Synephrine
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Product Name Synephrine
Price: $30 / 20mg
CAS No.: 94-07-5
Catalog No.: CFN99551
Molecular Formula: C9H13NO2
Molecular Weight: 167.21 g/mol
Purity: >=98%
Type of Compound: Alkaloids
Physical Desc.: White powder
Source: The young fruits Citrus aurantium L.
Solvent: Chloroform, Dichloromethane, Ethyl Acetate, DMSO, Acetone, etc.
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According to end customer requirements, ChemFaces provide solvent format. This solvent format of product intended use: Signaling Inhibitors, Biological activities or Pharmacological activities.
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Related Screening Libraries
Size /Price /Stock 10 mM * 100 uL in DMSO / Inquiry / In-stock
10 mM * 1 mL in DMSO / Inquiry / In-stock
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Biological Activity
Description: p-Synephrine is widely used in weight loss and weight management as well as in sports performance products, which has antidepressant-like effects in the murine models of forced swimming and tail suspension, it also exerts potent anti-inflammatory effects by inhibition of the NF-κB signaling pathway. Synephrine inhibits eotaxin-1 expression via the STAT6 signaling pathway.
Targets: STAT | IL Receptor | JAK | NF-kB | p65 | IkB | cAMP | Calcium Channel | IKK
In vitro:
Molecules. 2014 Aug 8;19(8):11883-95.
Synephrine inhibits eotaxin-1 expression via the STAT6 signaling pathway.[Pubmed: 25111027]
Citrus contain various flavonoids and alkaloids that have multiple biological activities. It is known that the immature Citrus contains larger amounts of bioactive components, than do the mature plants. Although Citrus flavonoids are well known for their biological activities, Citrus alkaloids have not previously been assessed.
METHODS AND RESULTS:
In this study, we identified Synephrine alkaloids as an active compound from immature Citrus unshiu, and investigated the effect of Synephrine on eotaxin-1 expression. Eotaxin-1 is a potent chemoattractant for eosinophils, and a critical mediator, during the development of eosinophilic inflammation. We found that Synephrine significantly inhibited IL-4-induced eotaxin-1 expression. This Synephrine effect was mediated through the inhibition of STAT6 phosphorylation in JAK/STAT signaling. We also found that eosinophil recruitment induced by eotaxin-1 overexpression was inhibited by Synephrine.
CONCLUSIONS:
Taken together, these findings indicate that inhibiting IL-4-induced eotaxin-1 expression by Synephrine occurs primarily through the suppression of eosinophil recruitment, which is mediated by inhibiting STAT6 phosphorylation.
Mol Cell Biochem. 2014 Mar;388(1-2):135-47.
The action of p-synephrine on hepatic carbohydrate metabolism and respiration occurs via both Ca(2+)-mobilization and cAMP production.[Pubmed: 24287564]
Citrus aurantium extracts, which contain large amounts of p-Synephrine, are widely used for weight loss purposes and as appetite suppressants. In the liver, C. aurantium (bitter orange) extracts affect hemodynamics, carbohydrate metabolism, and oxygen uptake. The purpose of the present work was to quantify the action of p-Synephrine and also to obtain indications about its mechanism of action, a task that would be difficult to accomplish with C. aurantium extracts due to their rather complex composition.
METHODS AND RESULTS:
The experimental system was the isolated perfused rat liver. p-Synephrine significantly stimulated glycogenolysis, glycolysis, gluconeogenesis, and oxygen uptake. The compound also increased the portal perfusion pressure and the redox state of the cytosolic NAD(+)/NADH couple. A Ca(2+)-dependency for both the hemodynamic and the metabolic effects of p-Synephrine was found. p-Synephrine stimulated both cAMP overflow and the initial Ca(2+) release from the cellular stores previously labeled with (45)Ca(2+). The metabolic and hemodynamic actions of p-Synephrine were strongly inhibited by α-adrenergic antagonists and moderately affected by β-adrenergic antagonists.
CONCLUSIONS:
The results allow to conclude that p-Synephrine presents important metabolic and hemodynamic effects in the liver. These effects can be considered as both catabolic (glycogenolysis) and anabolic (gluconeogenesis), they are mediated by both α- and β-adrenergic signaling, require the simultaneous participation of both Ca(2+) and cAMP, and could be contributing to the overall stimulation of metabolism that usually occurs during weight loss periods.
In vivo:
Inflamm Res. 2014 Jun;63(6):429-39.
p-Synephrine suppresses lipopolysaccharide-induced acute lung injury by inhibition of the NF-κB signaling pathway.[Pubmed: 24487736]
We investigated whether p-Synephrine exerts potent anti-inflammatory effects against acute lung injury (ALI) induced by lipopolysaccharide (LPS) in vivo, and we further investigated the inhibitory mechanism of p-Synephrine in LPS-induced ALI.
METHODS AND RESULTS:
Lipopolysaccharide (0.5 mg/kg) was instilled intranasally in phosphate-buffered saline to induce acute lung injury, and 6, 24, and 48 h after LPS was given, bronchoalveolar lavage fluid was obtained to measure pro-inflammatory mediator. We also evaluated the effects of p-Synephrine on LPS-induced the severity of pulmonary injury. The phosphorylation of nuclear factor-κB (NF-κB) p65 protein was analyzed by Western blotting. Our data showed that p-Synephrine significantly reduced the amount of inflammatory cells, the lung wet-to-dry weight (W/D) ratio, reactive oxygen species, myeloperoxidase activity and enhanced superoxide dismutase (SOD) in mice with LPS-induced ALI. Tumor necrosis factor α and interleukin (IL)-6 concentrations decreased significantly while the concentration of IL-10 was significantly increased after p-Synephrine pretreatment. In addition, p-Synephrine suppressed not only the phosphorylation of NF-κB but also the degradation of its inhibitor (IκBα).
CONCLUSIONS:
These results suggested that the inhibition of NF-κB activation and the regulation of SOD are involved in the mechanism of p-Synephrine's protection against ALI.
Synephrine Description
Source: The young fruits Citrus aurantium L.
Solvent: Chloroform, Dichloromethane, Ethyl Acetate, DMSO, Acetone, etc.
Storage: Providing storage is as stated on the product vial and the vial is kept tightly sealed, the product can be stored for up to 24 months(2-8C).

Wherever possible, you should prepare and use solutions on the same day. However, if you need to make up stock solutions in advance, we recommend that you store the solution as aliquots in tightly sealed vials at -20C. Generally, these will be useable for up to two weeks. Before use, and prior to opening the vial we recommend that you allow your product to equilibrate to room temperature for at least 1 hour.

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After receiving: The packaging of the product may have turned upside down during transportation, resulting in the natural compounds adhering to the neck or cap of the vial. take the vial out of its packaging and gently shake to let the compounds fall to the bottom of the vial. for liquid products, centrifuge at 200-500 RPM to gather the liquid at the bottom of the vial. try to avoid loss or contamination during handling.
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Recently, ChemFaces products have been cited in many studies from excellent and top scientific journals

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Calculate Dilution Ratios(Only for Reference)
1 mg 5 mg 10 mg 20 mg 25 mg
1 mM 5.9805 mL 29.9025 mL 59.805 mL 119.6101 mL 149.5126 mL
5 mM 1.1961 mL 5.9805 mL 11.961 mL 23.922 mL 29.9025 mL
10 mM 0.5981 mL 2.9903 mL 5.9805 mL 11.961 mL 14.9513 mL
50 mM 0.1196 mL 0.5981 mL 1.1961 mL 2.3922 mL 2.9903 mL
100 mM 0.0598 mL 0.299 mL 0.5981 mL 1.1961 mL 1.4951 mL
* Note: If you are in the process of experiment, it's need to make the dilution ratios of the samples. The dilution data of the sheet for your reference. Normally, it's can get a better solubility within lower of Concentrations.
Protocol
Animal Research:
Naunyn Schmiedebergs Arch Pharmacol. 2001 Jul;364(1):21-6.
Characterization of antidepressant-like effects of p-synephrine stereoisomers.[Pubmed: 11485034]
We previously reported that p-Synephrine has antidepressant-like activity in the murine models of forced swimming and tail suspension.
METHODS AND RESULTS:
In the present study, we characterized antidepressant-like effects of p-Synephrine stereoisomers in both in vivo and in vitro systems. In the tail suspension test, S-(+)-p-Synephrine (3 mg/kg, p.o.) reduced the duration of immobility, while R-(-)-p-Synephrine (0.3-3 mg/kg, p.o.) had no effect. S-(+)-p-Synephrine (0.3, 1 and 3 mg/kg, p.o.) and R-(-)-p-Synephrine (1 mg/ kg and 3 mg/kg, p.o.) significantly reversed the reserpine (2.5 mg/kg, i.p.)-induced hypothermia. S-(+)-p-Synephrine was more effective than R-(-)-p-Synephrine in inhibition of both [3H]noradrenaline uptake in rat cerebral cortical slices (maximal inhibition 85.7 +/- 7.8% vs. 59.8 +/- 4.3%; EC50 5.8 +/- 0.7 microM vs. 13.5 +/- 1.2 microM) and [3H]nisoxetine binding (Ki 4.5 +/- 0.5 microM vs. 8.2 +/- 0.7 microM). In contrast, R-(-)-p-Synephrine was more effective than S-(+)-p-Synephrine in stimulation of [3H]noradrenaline release from rat cerebral cortical slices (maximal stimulation 23.9 +/- 1.8% vs. 20.1 +/- 1.7%; EC50 8.2 +/- 0.6 microM vs. EC50 12.3 +/- 0.9 microM). The stimulatory effect of R-(-)-p-Synephrine on [3H]noradrenaline release was inhibited by nisoxetine (100 nM), but tetrodotoxin (1 microM) and elimination of extracellular calcium had no effect.
CONCLUSIONS:
It is suggested that S-(+)-p-Synephrine has more effective antidepressant-like activity than R-(-)-p-Synephrine.
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