p-Synephrine 

p-Synephrine is an orally active alkaloid dietary supplement without indirect sympathomimetic activity or cardiovascular stimulatory activity. p-Synephrine stimulates AMPK phosphorylation and mediates Glut4 translocation to increase glucose consumption and lactate production in skeletal muscle cells. p-Synephrine also downregulates the p38 MAPK and NF-κB signaling pathways to inhibit pro-inflammatory cytokine production and alter oxidative metabolism. p-Synephrine exhibits low subchronic toxicity in mice. p-Synephrine can be applied to research related to systemic inflammatory response syndrome, obesity, and type 2 diabetes^[1][2][3][4].

p-Synephrine (10 μg/mL) exerts lipolytic activity equivalent to 60% of that of isoproterenol in rat white adipocytes, and this proportion is 10% in human adipocytes^[1].
p-Synephrine activates glucose transport in human adipocytes^[1].
p-Synephrine binds to neuromedin U2 receptors in the HEK293 cell line with high efficiency and high affinity^[1].
p-Synephrine increases the basal glucose consumption of L6 skeletal muscle cells by more than 50% in a dose-dependent manner via AMP-activated protein kinase phosphorylation-mediated Glut4-dependent uptake, with no effect on cell viability^[1].
p-Synephrine reduces glucose production in H411E rat hepatocytes in a dose-dependent manner, and this effect is independent of α- and β-adrenergic receptor signaling pathways^[1].
p-Synephrine exerts anti-inflammatory effects in normal human fibroblasts and NIH/3 T3 mouse fibroblasts by inhibiting STAT6 phosphorylation to block IL-4-induced eotaxin-1 (eotaxin-1) expression^[1].
p-Synephrine inhibits inflammatory responses in LPS-stimulated RAW264.7 cells by downregulating the p38 MAPK and NF-κB signaling pathways via β-adrenergic receptors, thereby suppressing the production of proinflammatory cytokines and nitric oxide^[2].
p-Synephrine inhibits inflammatory responses in LPS-stimulated primary peritoneal macrophages by downregulating the p38 MAPK and NF-κB signaling pathways via β-adrenergic receptors, thereby suppressing the production of proinflammatory cytokines^[2].
p-Synephrine (0-100 μM; 24 h) does not affect the viability of differentiated L6 skeletal muscle myotubes, nor does it induce cytotoxicity in them^[4].
p-Synephrine (25-200 μM; 2 h) increases basal glucose consumption in differentiated L6 skeletal muscle myotubes in a dose-dependent manner, with the maximal effect observed at a concentration of 50 μM; it also enhances insulin-stimulated glucose consumption^[4].
p-Synephrine (25-50 μM; 7 h) increases both basal and insulin-stimulated lactate production in differentiated L6 skeletal muscle myotubes to more than 1.3-fold of the original levels^[4].
p-Synephrine (50 μM; 10 min) does not stimulate Akt phosphorylation at the Ser⁴⁷³ site, nor does it alter insulin-induced Akt phosphorylation, in differentiated L6 skeletal muscle myotubes^[4].
p-Synephrine (50 μM; 2 h) induces AMPK phosphorylation in differentiated L6 skeletal muscle myotubes, with greater potency than 1 mM AICAR^[4].
p-Synephrine (50 μM; 2 h) induces Glut4 translocation to the plasma membrane and stimulates glucose consumption in differentiated L6 skeletal muscle myotubes. Both of these effects depend on AMPK activity but are independent of PI3 kinase activity^[4].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

p-Synephrine suppresses lipopolysaccharide-induced acute lung injury in mice by reducing lung inflammation, oxidative stress, and pro-inflammatory cytokine levels while increasing anti-inflammatory cytokine levels^[1].
p-Synephrine exhibits antioxidant and tissue protective activities in normal mouse livers by modulating glutathione and antioxidant enzyme levels^[1].
p-Synephrine (30-300 mg/kg; p.o.; daily; 28 days) administered orally to healthy male CF1 mice for 28 days reduces body weight gain, alters oxidative stress biomarkers and shows low subchronic toxicity with no observed mortality or overt organ damage^[3].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

167.21

C₉H₁₃NO₂

614-35-7

Solid

White to off-white

OC1=CC=C([C@@H](O)CNC)C=C1

Room temperature in continental US; may vary elsewhere.

4°C, stored under nitrogen

*In solvent : -80°C, 6 months; -20°C, 1 month (stored under nitrogen)

* Please refer to the solubility information to select the appropriate solvent. Once prepared, please aliquot and store the solution to prevent product inactivation from repeated freeze-thaw cycles.
Storage method and period of stock solution: -80°C, 6 months; -20°C, 1 month (stored under nitrogen). When stored at -80°C, please use it within 6 months. When stored at -20°C, please use it within 1 month.

* Note: If you choose water as the stock solution, please dilute it to the working solution, then filter and sterilize it with a 0.22 μm filter before use.

• [1]. Stohs SJ, Shara M, Ray SD. p-Synephrine, ephedrine, p-octopamine and m-synephrine: Comparative mechanistic, physiological and pharmacological properties. Phytotherapy research : PTR. 2020 Aug;34(8):1838-1846.  [Content Brief]

  [2]. Ishida M, Takekuni C, Nishi K, et al.. -Synephrine suppresses inflammatory responses in lipopolysaccharide-stimulated RAW264.7 cells and alleviates systemic inflammatory response syndrome in mice. Food & function. 2022 May 10;13(9):5229-5239.  [Content Brief]

  [3]. Arbo MD, Schmitt GC, Limberger MF, et al.. Subchronic toxicity of Citrus aurantium L. (Rutaceae) extract and p-synephrine in mice. Regulatory toxicology and pharmacology : RTP. 2009 Jul;54(2):114-7.  [Content Brief]

  [4]. Hong NY, Cui ZG, Kang HK, et al.. p-Synephrine stimulates glucose consumption via AMPK in L6 skeletal muscle cells. Biochemical and biophysical research communications. 2012 Feb 24;418(4):720-4.  [Content Brief]