|Description:||1. (+)-Nortrachelogenin shows effects on the central nervous system producing depression in rabbits. |
2. (-)-Nortrachelogenin can induce membrane disruption and caspase-dependent apoptosis.
3. Nortrachelogenin shows anti-plasmodium activity of 14.50 dg/ml.
4. Nortrachelogenin has anti-inflammatory properties.
5. Nortrachelogenin is a novel agent for prostate cancer therapy with ability to inhibit Akt membrane localization and activity as well as the activation of growth factor receptors, thereby efficiently synergizing with tumor necrosis factor-related apoptosis-inducing ligand (TRAIL), exposure.
6. (-)-Nortrachelogenin exerts its antibacterial effect by disorganizing and perturbing the cytoplasmic membrane.
7. (+)-Nortrachelogenin is moderately active against HIV-1 in vitro.
8. Nortrachelogenin shows moderate inhibiting activities on NF- κB signaling pathway induced by TNFα , with the IC50 value of 49.4 uM.
|Targets:||Akt | IGF-1R | ROS | Caspase | NOS | PGE | NO | IL Receptor | COX | HIV | Antifection|
|Source:||The herbs of Trachelospermum jasminoides|
|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.
Need more advice on solubility, usage and handling? Please email to: email@example.com
|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.|
|1 mg||5 mg||10 mg||20 mg||25 mg|
|1 mM||2.6709 mL||13.3547 mL||26.7094 mL||53.4188 mL||66.7735 mL|
|5 mM||0.5342 mL||2.6709 mL||5.3419 mL||10.6838 mL||13.3547 mL|
|10 mM||0.2671 mL||1.3355 mL||2.6709 mL||5.3419 mL||6.6774 mL|
|50 mM||0.0534 mL||0.2671 mL||0.5342 mL||1.0684 mL||1.3355 mL|
|100 mM||0.0267 mL||0.1335 mL||0.2671 mL||0.5342 mL||0.6677 mL|
Biochem Pharmacol. 2013 Sep 1;86(5):571-83.
|The antitumor lignan Nortrachelogenin sensitizes prostate cancer cells to TRAIL-induced cell death by inhibition of the Akt pathway and growth factor signaling.[Pubmed: 23747345]|
|We report that the lignan Nortrachelogenin (NTG) is the most efficient of the 27 tested lignan compounds in sensitizing prostate cancer cells to TRAIL-induced apoptosis. Importantly, pretreatment with Nortrachelogenin does not sensitize a non-malignant prostate cell line to TRAIL-induced cell death. The structural comparison of lignans reveals that the dibenzylbutyrolactone skeleton is required for the apoptosis-sensitizing activity, while substitutions at the aromatic rings do not seem to play a critical role in this lignan function. Our study also characterizes the cellular effects and molecular mechanisms involved in Nortrachelogenin anticancer activity. We previously reported that specific lignans inhibit the Akt survival-signaling pathway in concert with TRAIL sensitization. While Nortrachelogenin is also shown to be a effective inhibitor of Akt signaling, in this study we further demonstrate that Nortrachelogenin potently inhibits tyrosine kinase (RTK) activation in response to growth factors, such as insulin and insulin-like growth factor I (IGF-I). Our results identify Nortrachelogenin as a novel agent for prostate cancer therapy with ability to inhibit Akt membrane localization and activity as well as the activation of growth factor receptors (GFRs), thereby efficiently synergizing with TRAIL exposure.|
J Nat Prod. 1979 Mar-Apr;42(2):159-62.
|(+)-Nortrachelogenin, a new pharmacologically active lignan from Wikstroemia indica.[Pubmed: 501363]|
|A new lignan, (+)-Nortrachelogenin (I), and a known compound, daphnoretin were isolated from Wikstroemia indica C. A. Meyer (Thymelaeaceae). The structure of (+)-Nortrachelogenin was established as 8(R), 8'(R)-4,4',8'-trihydroxy-3,3'-dimethoxylignan-olid(9, 9') on the basis of spectroscopic evidence and comparison with its enantiomer, (-)-Nortrachelogenin. (+)-Nortrachelogenin (I) showed effects on the central nervous system producing depression in rabbits.|
Int. J.Appl. Res.Nat.Prod.,2011,4(3):755-6.
|Anti-plasmodial activity of Nortrachelogenin from the root bark of Carissa edulis (vahl)[Reference: WebLink]|
|The decoction of the root bark of Carrisa edulis is used traditionally for treatment of malaria and other ailments. Plasmodium falcipurum in vitro drug sensitive study was conducted in order to evaluate the correlation between the ethno medicinal use and bioactivity of fractions and total extract of the plant. Methanolic extract of the root bark of carissa edulis showed anti-plasmodial activity against the chloroquin-senitive (D6) strains of plasmodium falciparum parasite with IC50 value of 1.95 Dg/ml. From this extract, a lignan compound Nortrachelogenin was isolated and showed anti-plasmodium activity of 14.50 Dg/ml. The structure was determined on the basis of spectroscopic evidence.|
FEMS Yeast Res. 2016 May;16(3).
|(-)-Nortrachelogenin from Partrinia scabiosaefolia elicits an apoptotic response in Candida albicans.[Pubmed: 26880798 ]|
|This study analyzes the antifungal properties of (-)-Nortrachelogenin and elucidates its mode of action against pathogenic fungi. We performed susceptibility tests against several pathogenic fungi and verified the absence of hemolysis against human erythrocytes. Its antifungal activity increased reactive oxygen species (ROS) in response to intracellular stress and increased concentrations of both intracellular and extracellular trehalose without causing hemolysis. In addition, a cell wall regeneration study indicated its action on the cytoplasmic membrane. A cell surface study using 3,3(')-dipropylthiacarbocyanine iodide [DiSC3(5)] and 1,6-diphenyl-1,3,5-hexatriene (DPH) demonstrated dissipation of the cytoplasmic membrane at high concentrations. Our study revealed a disturbance in the membrane at higher concentrations and externalization of phosphatidylserine in a dose-dependent manner, affecting other intracellular responses. Furthermore, we investigated the late stage of apoptosis using TUNEL and 4('),6-diamidino-2-phenylindole (DAPI) assays. (-)-Nortrachelogenin-treated cells underwent apoptosis which was triggered by mitochondrial dysfunction via depolarization of the mitochondrial membrane, release of cytochrome c and calcium ion signaling, resulting in the activation of metacaspases. Different concentrations of (-)-Nortrachelogenin induced membrane disruption and caspase-dependent apoptosis.|
Planta Med. 2017 Apr;83(6):519-526.
|Anti-inflammatory Effects of Nortrachelogenin in Murine J774 Macrophages and in Carrageenan-Induced Paw Edema Model in the Mouse.[Pubmed: 27737478 ]|
|Nortrachelogenin is a pharmacologically active lignan found in knot extracts of Pinus sylvestris. In previous studies, some lignans have been shown to have anti-inflammatory properties, which made Nortrachelogenin an interesting candidate for our study. In inflammation, bacterial products and cytokines induce the expression of inducible nitric oxide synthase, cyclooxygenase-2, and microsomal prostaglandin E synthase-1. These enzymes synthesize factors, which, together with proinflammatory cytokines, are important mediators and drug targets in inflammatory diseases.The effects of Nortrachelogenin on the expression of inducible nitric oxide synthase, cyclooxygenase-2, and microsomal prostaglandin E synthase-1 as well as on the production of nitric oxide, prostaglandin E2, and cytokines interleukin-6 and monocyte chemotactic protein-1 were investigated in the murine J774 macrophage cell line. In addition, we examined the effect of Nortrachelogenin on carrageenan-induced paw inflammation in mice.Interestingly, Nortrachelogenin reduced carrageenan-induced paw inflammation in mice and inhibited the production of inflammatory factors nitric oxide, prostaglandin E2, interleukin-6, and monocyte chemotactic protein-1 in J774 macrophages in vitro. Nortrachelogenin inhibited microsomal prostaglandin E synthase-1 protein expression but had no effect on cyclooxygenase-2 protein levels. Nortrachelogenin also had a clear inhibitory effect on inducible nitric oxide synthase protein expression but none on its mRNA levels, and the proteasome inhibitor lactacystin reversed the effect of Nortrachelogenin on inducible nitric oxide synthase expression, suggesting a post-transcriptional mechanism of action.The results revealed hitherto unknown anti-inflammatory properties of Nortrachelogenin, which could be utilized in the development of anti-inflammatory treatments.|
Curr Microbiol. 2016 Jan;72(1):48-54.
|Antibacterial Mechanism of (-)-Nortrachelogenin in Escherichia coli O157.[Pubmed: 26420306 ]|
|(-)-Nortrachelogenin is a lignan belonging to group of polyphenolic compounds. Its biological properties in mammalian cells are well-studied; however, its biological effects in microorganisms remain poorly understood. Its efficacy against pathogenic bacteria, including antibiotic-resistant strains, was investigated and it was found that bacteria are highly susceptible to the antibacterial effects of this compound. To investigate the antibacterial mode of action(s) against Escherichia coli O157, its effect on the penetration of SYTOX green into bacterial cells was assayed. The penetration of SYTOX Green into a bacterial cell is a measure of permeability of the plasma membrane. An increase in fluorescence intensity using bis-(1,3-dibutylbarbituric acid) trimethine oxonol [DiBAC4(3)] and 3,3'-dipropylthiacarbocyanine iodide [DiSC3(5)] was also observed, indicating membrane depolarization. Potassium ion efflux from the cytosol into the extracellular matrix showed that cellular damage due to (-)-Nortrachelogenin treatment resulted in the loss of intracellular components. While cells were damaged by (-)-Nortrachelogenin, large unilamellar vesicles containing fluorescein isothiocyanate-dextran were perturbed to migrate molecules between 3.3 and 4.8 nm. The release of calcein from giant unilamellar vesicles, occurring as a result of disruption in artificial membranes, was visualized. Taken together, our results indicate that (-)-Nortrachelogenin exerts its antibacterial effect by disorganizing and perturbing the cytoplasmic membrane, demonstrating the potential of this compound as a candidate for antibiotic drug development.|
Planta Med. 2000 Aug;66(6):564-7.
|Antifungal, antimitotic and anti-HIV-1 agents from the roots of Wikstroemia indica.[Pubmed: 10985087 ]|
|With guidance of Pyricularia oryzae bioassay, daphnoretin (1), (+)-Nortrachelogenin (2), genkwanol A (3), wikstrol A (4), wikstrol B (5) and daphnodorin B (6) were isolated from the roots of Wikstroemia indica. Compounds 1-6 induced morphological deformation of P. oryzae mycelia with MMDC values of 68.4 +/- 1.3, 31.3 +/- 1.8, 45.8 +/- 0.5, 70.1 +/- 2.4, 52.3 +/- 0.9 and 73.7 +/- 1.6 microM, respectively. Compounds 3-6 showed moderate activity against microtubule polymerization with IC50 values of 112 +/- 4, 131 +/- 3, 184 +/- 6 and 142 +/- 2 microM in vitro, respectively. Compounds 2, 3, 5 and 6 were moderately active against HIV-1 in vitro. The findings of bioactivity of 1-6 support the antifungus, antimitosis and anti-HIV-1 uses for W. indica roots.|