RhynchophyllineCAS# 76-66-4 |
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Quality Control & MSDS
Number of papers citing our products
Chemical structure
3D structure
Cas No. | 76-66-4 | SDF | Download SDF |
PubChem ID | 5281408 | Appearance | White powder |
Formula | C22H28N2O4 | M.Wt | 384.47 |
Type of Compound | Alkaloids | Storage | Desiccate at -20°C |
Synonyms | Mitrinermine | ||
Solubility | DMSO : 33.33 mg/mL (86.69 mM; Need ultrasonic) H2O : < 0.1 mg/mL (insoluble) | ||
Chemical Name | methyl (E)-2-[(3R,6'R,7'S,8'aS)-6'-ethyl-2-oxospiro[1H-indole-3,1'-3,5,6,7,8,8a-hexahydro-2H-indolizine]-7'-yl]-3-methoxyprop-2-enoate | ||
SMILES | CCC1CN2CCC3(C2CC1C(=COC)C(=O)OC)C4=CC=CC=C4NC3=O | ||
Standard InChIKey | DAXYUDFNWXHGBE-KAXDATADSA-N | ||
Standard InChI | InChI=1S/C22H28N2O4/c1-4-14-12-24-10-9-22(17-7-5-6-8-18(17)23-21(22)26)19(24)11-15(14)16(13-27-2)20(25)28-3/h5-8,13-15,19H,4,9-12H2,1-3H3,(H,23,26)/b16-13+/t14-,15-,19-,22+/m0/s1 | ||
General tips | For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.Stock solution can be stored below -20℃ for several months. We recommend that you prepare and use the solution on the same day. However, if the test schedule requires, the stock solutions can be prepared in advance, and the stock solution must be sealed and stored below -20℃. In general, the stock solution can be kept for several months. Before use, we recommend that you leave the vial at room temperature for at least an hour before opening it. |
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About Packaging | 1. The packaging of the product may be reversed during transportation, cause the high purity compounds to adhere to the neck or cap of the vial.Take the vail out of its packaging and shake gently until the compounds fall to the bottom of the vial. 2. For liquid products, please centrifuge at 500xg to gather the liquid to the bottom of the vial. 3. Try to avoid loss or contamination during the experiment. |
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Shipping Condition | Packaging according to customer requirements(5mg, 10mg, 20mg and more). Ship via FedEx, DHL, UPS, EMS or other couriers with RT, or blue ice upon request. |
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 | Effects of rhynchophylline on GluN1 and GluN2B expressions in primary cultured hippocampal neurons.[Pubmed: 25110195]Fitoterapia. 2014 Oct;98:166-73.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. Rhynchophylline attenuates LPS-induced pro-inflammatory responses through down-regulation of MAPK/NF-κB signaling pathways in primary microglia.[Pubmed: 22322985 ]Phytother Res. 2012 Oct;26(10):1528-33.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. |
In vivo | Uncaria rhynchophylla and Rhynchophylline inhibit c-Jun N-terminal kinase phosphorylation and nuclear factor-kappaB activity in kainic acid-treated rats.[Pubmed: 19507277 ]Am J Chin Med. 2009;37(2):351-60.Our previous studies have shown that Uncaria rhynchophylla (UR) can reduce epileptic seizures. |
Kinase Assay | Rhynchophylline and isorhynchophylline inhibit NMDA receptors expressed in Xenopus oocytes.[Pubmed: 12433591]Effect of rhynchophylline on platelet aggregation and cytoplasmic free calcium level in rabbits.[Reference: WebLink]Chinese Journal of Pharmacology & Toxicology, 2011, 25(1):68-71.
Eur J Pharmacol. 2002 Nov 22;455(1):27-34.Rhynchophylline and isoRhynchophylline are major tetracyclic oxindole alkaloid components of Uncaira species, which have been long used as medicinal plants. |
Animal Research | Antihypertensive effect and vascular regulation mechanism of rhynchophylline on spontaneously hypertensive rats[Reference: WebLink]Rhynchophylline prevents cardiac dysfunction and improves survival in lipopolysaccharide-challenged mice via suppressing macrophage I-κBα phosphorylation.[Pubmed: 22841535 ]Int Immunopharmacol. 2012 Nov;14(3):243-51.The purpose of the present study is to investigate the effect of Rhynchophylline (Rhy) on LPS-induced myocardial dysfunction in mice. Chinese Traditional & Herbal Drugs, 2014, 45(15): 2210-3.
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Rhynchophylline Dilution Calculator
Rhynchophylline Molarity Calculator
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 necessary to make the dilution ratios of the samples. The dilution data above is only for reference. Normally, it's can get a better solubility within lower of Concentrations. |
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Rhyncholphylline, an alkaloid isolated from Uncaria, shows potent inhibition of lipopolysaccharide (LPS)-induced NO production in rat primary microglial cells. IC50 value: Target: In vitro: Rhyncholphylline effectively suppresses release of proinflammatory cytokines in LPS-activated microglial cells and the underling molecular mechanism for the inhibition of microglial activation; Attenuated LPS-induced production of proinflammatory cytokines such as TNF-α and IL-1β as well as NO in mouse N9 microglial cells [1]. Rhynchophylline exerts it protective action against ischemia-induced neuronal damage by preventing NMDA, muscarinic M1, and 5-HT2 receptors-mediated neurotoxicity during ischemia [3]. In vivo: The neuroprotective effect of rhynchophylline was investigated in a stroke model. Following pMCAO, rhynchophylline treatment not only ameliorated neurological deficits, infarct volume and brain edema, but also increased claudin-5 and BDNF expressions (p < 0.05). Moreover, rhynchophylline could activate PI3K/Akt/mTOR signaling while inhibiting TLRs/NF-κB pathway [2].
References:
[1]. Dan Yuan, et al. Anti-inflammatory effects of rhynchophylline and isorhynchophylline in mouse N9 microglial cells and the molecular mechanism. International Immunopharmacology Volume 9, Issues 13–14, December 2009, Pages 1549–1554
[2]. Houcai Huang, et al. Neuroprotective Effects of Rhynchophylline Against Ischemic Brain Injury via Regulation of the Akt/mTOR and TLRs Signaling Pathways. Molecules 2014, 19 (8): 11196-11210; doi:10.3390/molecules190811196
[3]. Tai-Hyun Kang, et al. Protective effect of rhynchophylline and isorhynchophylline on in vitro ischemia-induced neuronal damage in the hippocampus: putative neurotransmitter receptors involved in their action. Life Sciences Volume 76, Issue 3, 3 December
[4]. Kinzo Matsumoto, et al. Suppressive effects of isorhynchophylline on 5-HT2A receptor function in the brain: Behavioural and electrophysiological studies. European Journal of Pharmacology Volume 517, Issue 3, 11 July 2005, Pages 191–199
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Uncaria rhynchophylla and Rhynchophylline inhibit c-Jun N-terminal kinase phosphorylation and nuclear factor-kappaB activity in kainic acid-treated rats.[Pubmed:19507277]
Am J Chin Med. 2009;37(2):351-60.
Our previous studies have shown that Uncaria rhynchophylla (UR) can reduce epileptic seizures. 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. 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.
Effects of rhynchophylline on GluN1 and GluN2B expressions in primary cultured hippocampal neurons.[Pubmed:25110195]
Fitoterapia. 2014 Oct;98:166-73.
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. 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 mumol/L) and MK-801 (lower than 200 mumol/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. These findings show that Rhynchophylline reciprocally regulates GluN1 and GluN2B expressions in hippocampal neurons, indicating a potential anxiolytic property for Rhynchophylline.
Rhynchophylline attenuates LPS-induced pro-inflammatory responses through down-regulation of MAPK/NF-kappaB signaling pathways in primary microglia.[Pubmed:22322985]
Phytother Res. 2012 Oct;26(10):1528-33.
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. 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-alpha (TNF-alpha) and interleukin-1beta (IL-1beta) 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 IkappaBalpha phosphorylation and degradation, inhibited the phosphorylation of mitogen-activated protein kinases (MAPKs). 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.
Rhynchophylline and isorhynchophylline inhibit NMDA receptors expressed in Xenopus oocytes.[Pubmed:12433591]
Eur J Pharmacol. 2002 Nov 22;455(1):27-34.
Rhynchophylline and isoRhynchophylline are major tetracyclic oxindole alkaloid components of Uncaira species, which have been long used as medicinal plants. 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. 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.
Rhynchophylline prevents cardiac dysfunction and improves survival in lipopolysaccharide-challenged mice via suppressing macrophage I-kappaBalpha phosphorylation.[Pubmed:22841535]
Int Immunopharmacol. 2012 Nov;14(3):243-51.
Myocardial dysfunction is a common complication during sepsis and significantly contributes to the mortality of patients with septic shock. However, none of the available therapeutic strategies proven to be effective in patients with severe sepsis are designed specifically to target myocardial dysfunction. The purpose of the present study is to investigate the effect of Rhynchophylline (Rhy) on LPS-induced myocardial dysfunction in mice. 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-kappaBalpha (I-kappaBalpha) phosphorylation, tumor necrosis factor-alpha (TNF-alpha) and interleukin-1beta (IL-1beta) mRNA expression, and in turn increased cardiac TNF-alpha and IL-1beta protein production, all of which were attenuated by pretreatment with Rhy. Immunohistochemistry revealed that TNF-alpha was found in infiltrated macrophages (F4/80(+)) and myocardium, and Rhy reduced TNF-alpha immunostaining in cardiac infiltrated macrophages in LPS-challenged mice. Furthermore, Rhy inhibited LPS-induced I-kappaBalpha phosphorylation and TNF-alpha production in cultured mouse peritoneal macrophages, but not in neonatal mouse cardiomyocytes. Pretreatment with Rhy significantly decreased the mortality of LPS-challenged mice. These results indicate that Rhy reduces cardiac dysfunction and improves survival via suppression of macrophage I-kappaBalpha phosphorylation in LPS-challenged mice, and suggest that Rhy may be a potential agent for the treatment of septic cardiac dysfunction.