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Rhynchophylline
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Product Name Rhynchophylline
Price: $98 / 20mg
CAS No.: 76-66-4
Catalog No.: CFN98131
Molecular Formula: C22H28N2O4
Molecular Weight: 384.47 g/mol
Purity: >=98%
Type of Compound: Alkaloids
Physical Desc.: Powder
Source: The herbs of Uncaria rhynchophylla.
Solvent: Chloroform, Dichloromethane, Ethyl Acetate, DMSO, Acetone, etc.
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Related Screening Libraries
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Biological Activity
Description: Rhynchophylline, a noncompetitive antagonist of the NMDA receptor, which has anti-inflammatory, anti-hypertension, cardiacprotective and neuroprotective activities. Rhynchophylline can markedly inhibit rabbit platelet aggregation induced by ADP or thrombin possibly by depressing the inflow of Ca2+ and the rise of the cytoplasmic free calcium level in platelet.Rhynchophylline can reduce the systolic blood pressure (SBP) of spontaneously hypertensive rats (SHR) significantly, decrease plasma Ang II, ADMA, and AT1R levels, and promote serum NO and NOS levels, which has the protection of vascular endothelial function.
Targets: NO | PGE | TNF-α | NOS | COX | IL Receptor | MAPK | IkB | AP-1 | JNK | NF-kB | NMDAR | IKK
In vitro:
Fitoterapia. 2014 Oct;98:166-73.
Effects of rhynchophylline on GluN1 and GluN2B expressions in primary cultured hippocampal neurons.[Pubmed: 25110195]
N-methyl-d-aspartate (NMDA) receptor subunits GluN1 and GluN2B in hippocampal neurons play key roles in anxiety. Our previous studies show that Rhynchophylline, an active component of the Uncaria species, down-regulates GluN2B expression in the hippocampal CA1 area of amphetamine-induced rat.
METHODS AND RESULTS:
The effects of Rhynchophylline on expressions of GluN1 and GluN2B in primary hippocampal neurons in neonatal rats in vitro were investigated. Neonatal hippocampal neurons were cultured with neurobasal-A medium. After incubation for 6h or 48 h with Rhynchophylline (non-competitive NMDAR antagonist) and MK-801 (non-competitive NMDAR antagonist with anxiolytic effect, as the control drug) from day 6, neuron toxicity, mRNA and protein expressions of GluN1 and GluN2B were analyzed. GluN1 is mainly distributed on neuronal axons and dendritic trunks, cytoplasm and cell membrane near axons and dendrites. GluN2B is mainly distributed on the membrane, dendrites, and axon membranes. GluN1 and GluN2B are codistributed on dendritic trunks and dendritic spines. After 48 h incubation, a lower concentration of Rhynchophylline (lower than 400 μmol/L) and MK-801 (lower than 200 μmol/L) have no toxicity on neonatal hippocampal neurons. Rhynchophylline up-regulated GluN1 mRNA expression at 6h and mRNA and protein expressions at 48h, but down-regulated GluN2B mRNA and protein expressions at 48 h. However, GluN1 and GluN2B mRNA expressions were down-regulated at 6h, and mRNA and protein expressions were both up-regulated by MK-801 at 48h.
CONCLUSIONS:
These findings show that Rhynchophylline reciprocally regulates GluN1 and GluN2B expressions in hippocampal neurons, indicating a potential anxiolytic property for Rhynchophylline.
Phytother Res. 2012 Oct;26(10):1528-33.
Rhynchophylline attenuates LPS-induced pro-inflammatory responses through down-regulation of MAPK/NF-κB signaling pathways in primary microglia.[Pubmed: 22322985 ]
Excessive activation of microglial cells has been implicated in various types of neuroinflammation. Suppression of microglial activation would have therapeutic benefits, leading to the alleviation of the progression of neurodegeneration.
METHODS AND RESULTS:
In this study, the inhibitory effects of Rhynchophylline (RIN), a tetracyclic oxindole alkaloid component isolated from Uncaria rhynchophylla (Miq.) Jacks., on the production of pro-inflammatory mediators were investigated in lipopolysaccharide (LPS)-stimulated microglia. The results showed that RIN markedly reduced the production of nitric oxide (NO), prostaglandins E(2) (PGE(2) ), monocyte chemoattractant protein (MCP-1), tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β) in LPS-activated microglia. The mRNA expression levels of iNOS and COX-2 were also depressed by RIN in a concentration-dependent manner. Further studies revealed that RIN blocked IκBα phosphorylation and degradation, inhibited the phosphorylation of mitogen-activated protein kinases (MAPKs).
CONCLUSIONS:
In summary, these data suggest that RIN suppresses inflammatory responses of microglia and may act as a potential therapeutic agent for various neurodegenerative diseases involving neuroinflammation.
In vivo:
Am J Chin Med. 2009;37(2):351-60.
Uncaria rhynchophylla and Rhynchophylline inhibit c-Jun N-terminal kinase phosphorylation and nuclear factor-kappaB activity in kainic acid-treated rats.[Pubmed: 19507277 ]
Our previous studies have shown that Uncaria rhynchophylla (UR) can reduce epileptic seizures.
METHODS AND RESULTS:
We hypothesized that UR and its major component Rhynchophylline (RH), reduce epileptic seizures in rats treated with kainic acid (KA) by inhibiting nuclear factor-kappaB (NF-kappaB) and activator-protein-1 (AP-1) activity, and by eliminating superoxide anions. Therefore, the level of superoxide anions and the DNA binding activities of NF-kappaB and AP-1 were measured. Sprague-Dawley (SD) rats were pre-treated with UR (1.0 g/kg, i.p.), RH (0.25 mg/kg, i.p.), or valproic acid (VA, 250 mg/kg, i.p.) for 3 days and then KA was administered intra-peritoneal (i.p.). The results indicated that UR, RH, and VA can reduce epileptic seizures and the level of superoxide anions in the blood. Furthermore, KA was demonstrated to induce the DNA binding activities of NF-kappaB and AP-1. However, these inductions were inhibited by pre-treatment with UR, RH, or VA for 3 days. Moreover, UR and RH were shown to be involved in the suppression of c-Jun N-terminal kinase (JNK) phosphorylation.
CONCLUSIONS:
This study suggested that UR and RH have antiepileptic effects in KA-induced seizures and are associated with the regulation of the innate immune system via a reduction in the level of superoxide anions, JNK phosphorylation, and NF-kappaB activation.
Rhynchophylline Description
Source: The herbs of Uncaria rhynchophylla.
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 2.601 mL 13.0049 mL 26.0098 mL 52.0197 mL 65.0246 mL
5 mM 0.5202 mL 2.601 mL 5.202 mL 10.4039 mL 13.0049 mL
10 mM 0.2601 mL 1.3005 mL 2.601 mL 5.202 mL 6.5025 mL
50 mM 0.052 mL 0.2601 mL 0.5202 mL 1.0404 mL 1.3005 mL
100 mM 0.026 mL 0.13 mL 0.2601 mL 0.5202 mL 0.6502 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
Kinase Assay:
Chinese Journal of Pharmacology & Toxicology, 2011, 25(1):68-71.
Effect of rhynchophylline on platelet aggregation and cytoplasmic free calcium level in rabbits.[Reference: WebLink]

METHODS AND RESULTS:
After Rhynchophylline (Rhy) 0.65 and 1.30 mmol·L-1 were administered, the cytoplasmic free calcium level induced by ADP decreased to 620 ± 37 and (528 ± 17) nmol·L-1, respectively (P < 0.05), the cytoplasmic free calcium level induced by thrombin decreased to 777 ±29 and (658 ±23) nmol·L-1, respectively (P < 0.05). In the absence of extracellular Ca+, Rhy had no significant influence on cytoplasmic free calcium level of rabbit platelet.
CONCLUSIONS:
Rhy markedly inhibits rabbit platelet aggregation induced by ADP or thrombin possibly by depressing the inflow of Ca+ and the rise of the cytoplasmic free calcium level in platelet.
Eur J Pharmacol. 2002 Nov 22;455(1):27-34.
Rhynchophylline and isorhynchophylline inhibit NMDA receptors expressed in Xenopus oocytes.[Pubmed: 12433591]
Rhynchophylline and isoRhynchophylline are major tetracyclic oxindole alkaloid components of Uncaira species, which have been long used as medicinal plants.
METHODS AND RESULTS:
In this study, the effects of Rhynchophylline and isoRhynchophylline on the ionotropic and metabotropic glutamate receptor-mediated current responses were examined using Xenopus oocytes injected with total RNA prepared from rat cortices or cerebelli. Rhynchophylline and isoRhynchophylline (1-100 microM) per se failed to induce membrane current, but these alkaloids reversibly reduced N-methyl-D-aspartate (NMDA)-induced current in a concentration-dependent but voltage-independent manner. The IC(50) values of Rhynchophylline and isoRhynchophylline were 43.2 and 48.3 microM, respectively. Substitution of Ba(2+) for Ca(2+) in the recording medium did not alter the extent of Rhynchophylline- and isoRhynchophylline-induced suppression of NMDA currents. In contrast, neither alkaloid had an effect on the currents mediated by ionotropic kainic acid-type and (+/-)-alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA)-type glutamate receptors or by the metabotropic glutamate receptor(1 and 5) (mGlu(1/5)). Rhynchophylline and isoRhynchophylline (30 microM) significantly reduced the maximal current responses evoked by NMDA and glycine (a co-agonist of NMDA receptor), but had no effect on the EC(50) values and Hill coefficients of NMDA and glycine for inducing currents. These alkaloids showed no interaction with the polyamine binding site, the Zn(2+) site, proton site or redox modulatory site on the NMDA receptor.
CONCLUSIONS:
These results suggest that Rhynchophylline and isoRhynchophylline act as noncompetitive antagonists of the NMDA receptor and that this property may contribute to the neuroprotective and anticonvulsant activity of the Uncaira species plant extracts.
Animal Research:
Int Immunopharmacol. 2012 Nov;14(3):243-51.
Rhynchophylline prevents cardiac dysfunction and improves survival in lipopolysaccharide-challenged mice via suppressing macrophage I-κBα phosphorylation.[Pubmed: 22841535 ]
The purpose of the present study is to investigate the effect of Rhynchophylline (Rhy) on LPS-induced myocardial dysfunction in mice.
METHODS AND RESULTS:
We found that pretreatment with Rhy significantly improved cardiac systolic dysfunction, increased stroke volume and cardiac output in mice challenged with LPS. LPS induced cardiac inhibitor-κBα (I-κBα) phosphorylation, tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β) mRNA expression, and in turn increased cardiac TNF-α and IL-1β protein production, all of which were attenuated by pretreatment with Rhy. Immunohistochemistry revealed that TNF-α was found in infiltrated macrophages (F4/80(+)) and myocardium, and Rhy reduced TNF-α immunostaining in cardiac infiltrated macrophages in LPS-challenged mice. Furthermore, Rhy inhibited LPS-induced I-κBα phosphorylation and TNF-α production in cultured mouse peritoneal macrophages, but not in neonatal mouse cardiomyocytes. Pretreatment with Rhy significantly decreased the mortality of LPS-challenged mice.
CONCLUSIONS:
These results indicate that Rhy reduces cardiac dysfunction and improves survival via suppression of macrophage I-κBα phosphorylation in LPS-challenged mice, and suggest that Rhy may be a potential agent for the treatment of septic cardiac dysfunction.
Chinese Traditional & Herbal Drugs, 2014, 45(15): 2210-3.
Antihypertensive effect and vascular regulation mechanism of rhynchophylline on spontaneously hypertensive rats[Reference: WebLink]

METHODS AND RESULTS:
SHR were randomly divided into model, positive control(Captopril 6.25 mg/kg), low-, mid-, and high-dose(1.25, 2.50, 5.00 mg/kg) Rhy groups. Other SD rats were included as the control group. Rats in the model and control groups were given the same volume of distilled water once daily for 21 d. Rat tail artery SBP was measured before administration and day 7, 14, and 21 during the administration. The levels of plasma Ang II, ADMA, AT1 R, and serum NO, NOS were detected after the last administration underwent blood sampling. Compared with the model group, Rhynchophylline(Rhy) reduced SBP significantly. Moreover, the plasma Ang II, ADMA, and AT1 R levels were up-regulated, and the serum NO and NOS levels were decreased in the model group, which could be reversed by the treatment of Rhy(P 0.05, 0.01).
CONCLUSIONS:
Rhy could reduce the SBP of SHR significantly, decrease plasma Ang II, ADMA, and AT1 R levels, and promote serum NO and NOS levels, which has the protection of vascular endothelial function.
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