TephrosinCAS# 76-80-2 |
Quality Control & MSDS
Number of papers citing our products
Chemical structure
3D structure
| Cas No. | 76-80-2 | SDF | Download SDF |
| PubChem ID | 114909 | Appearance | Cryst. |
| Formula | C23H22O7 | M.Wt | 410.43 |
| Type of Compound | Flavonoids | Storage | Desiccate at -20°C |
| Solubility | Soluble in Chloroform,Dichloromethane,Ethyl Acetate,DMSO,Acetone,etc. | ||
| SMILES | CC1(C=CC2=C(O1)C=CC3=C2OC4COC5=CC(=C(C=C5C4(C3=O)O)OC)OC)C | ||
| Standard InChIKey | AQBZCCQCDWNNJQ-AUSIDOKSSA-N | ||
| Standard InChI | InChI=1S/C23H22O7/c1-22(2)8-7-12-15(30-22)6-5-13-20(12)29-19-11-28-16-10-18(27-4)17(26-3)9-14(16)23(19,25)21(13)24/h5-10,19,25H,11H2,1-4H3/t19-,23-/m1/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 | 1. Tephrosin may be valuable for augmenting the therapeutic efficacy of 2-Deoxy-D-glucose(DG), DG is currently under clinical evaluation for targeting tumor cells. 2. Tephrosin has potent antitumor activity by inducing autophagy pathway, internalization and degradation of inactivated EGFR and ErbB2. 3. Tephrosin could exert antitumor effects by inducing internalization and degradation of inactivated EGFR and ErbB2 in human colon cancer cells. |
| Targets | ROS | PARP | Autophagy | HSP (e.g. HSP90) | EGFR | Akt | ERK | Caspase | AMPK | mTOR |
Tephrosin Dilution Calculator
Tephrosin Molarity Calculator
| 1 mg | 5 mg | 10 mg | 20 mg | 25 mg | |
| 1 mM | 2.4365 mL | 12.1823 mL | 24.3647 mL | 48.7294 mL | 60.9117 mL |
| 5 mM | 0.4873 mL | 2.4365 mL | 4.8729 mL | 9.7459 mL | 12.1823 mL |
| 10 mM | 0.2436 mL | 1.2182 mL | 2.4365 mL | 4.8729 mL | 6.0912 mL |
| 50 mM | 0.0487 mL | 0.2436 mL | 0.4873 mL | 0.9746 mL | 1.2182 mL |
| 100 mM | 0.0244 mL | 0.1218 mL | 0.2436 mL | 0.4873 mL | 0.6091 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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Tephrosin-induced autophagic cell death in A549 non-small cell lung cancer cells.[Pubmed:21061222]
J Asian Nat Prod Res. 2010 Nov;12(11):992-1000.
Anticancer effect of Tephrosin (1) has been documented; however, the molecular mechanisms underlying the cytotoxicity of Tephrosin in cancer cells remain unclear. In the present paper, the proliferation inhibition rate of several cancer cells was tested using the MTT assay; cell cycle, reactive oxygen species (ROS), and mitochondrial membrane potential (MMP) were determined by flow cytometry; poly(ADP-ribose) polymerase (PARP) cleavage and heat shock protein 90 (Hsp90) expression were evaluated by Western blotting; autophagy was examined by confocal microscopy and light chain 3 (LC3) conversion assay. The results showed that exposure of the cells to Tephrosin induced significant proliferation inhibition in a dose-dependent manner, especially on A549 with G(2)/M being arrested. Tephrosin was not found to induce cell apoptosis as PARP cleavage was not detected after 24 h treatment, but the formation of acidic vesicular organelle of autophagy character was found, and autophagy was further confirmed by the increase in the ratio of LC3-II to LC3-I. It was observed that Tephrosin induced ROS generation and Hsp90 expression inhibition. These results indicate that Tephrosin induces A549 cancer cell death via the autophagy pathway, and the roles of ROS generation and Hsp90 expression inhibition in this process need further study in the future.
Tephrosin induces internalization and degradation of EGFR and ErbB2 in HT-29 human colon cancer cells.[Pubmed:20056314]
Cancer Lett. 2010 Jul 1;293(1):23-30.
Inactivation of epidermal growth factor receptor (EGFR) family members are prime targets for cancer therapy. Here, we show that Tephrosin, a natural rotenoid which has potent antitumor activities, induced internalization of EGFR and ErbB2, and thereby induced degradation of the receptors. Treatment of HT-29 cells with Tephrosin inhibited both the ligand-induced and constitutive phosphorylation of EGFR, ErbB2 and ErbB3, and concomitantly suppressed the activation of the downstream signaling molecules such as Akt and Erk1/2 mitogen-activated protein kinase (MAPK). Tephrosin caused internalization of EGFR and ErbB2 into vehicles, which resulted in degradation of the receptors. This degradation was blocked by the lysosomal inhibitor, chloroquine. We also showed that Tephrosin induced apoptosis. Tephrosin did not induce the proteolytic processing of caspase-3 and poly(ADP-ribose) polymerase (PARP), but did nuclear translocation of apoptosis-inducing factor (AIF), suggesting that Tephrosin may induce caspase-independent apoptosis. These findings provide the first evidence that Tephrosin could exert antitumor effects by inducing internalization and degradation of inactivated EGFR and ErbB2 in human colon cancer cells.
The combination of tephrosin with 2-deoxy-D-glucose enhances the cytotoxicity via accelerating ATP depletion and blunting autophagy in human cancer cells.[Pubmed:22123175]
Cancer Biol Ther. 2011 Dec 1;12(11):989-96.
2-Deoxy-D-glucose (2-DG), a synthetic glucose analog that acts as a glycolytic inhibitor, is currently under clinical evaluation for targeting tumor cells. Tephrosin (TSN), a plant rotenoid, is known as an anticancer agent. In this study, we describe that the addition of TSN to 2-DG enhanced the cytotoxic activity of 2-DG against various types of cancer cells by accelerating ATP depletion and blunting autophagy. TSN increased the sensitivity of cancer cells to the cytotoxic effect of 2-DG. The combination of TSN and 2-DG induced acceleration of intracellular ATP depletion and the drastic activation of AMP-activated protein kinase (AMPK), which resulted in the inactivation of the mammalian target of rapamycin (mTOR) pathway. Of particular interest, TSN suppressed 2-DG-induced autophagy, a cell survival process in response to nutrient deprivation. We also showed that TSN inhibited 2-DG-induced activation of elongation factor-2 kinase (eEF-2K), which has been known to regulate 2-DG-induced autophagy. Inhibition of eEF-2K by RNA interference blunted 2-DG-induced autophagy and increased the sensitivity of cancer cells to the cytotoxic effect of 2-DG. The addition of TSN to 2-DG, however, did not enhance the cytotoxic activity of 2-DG by knockdown of eEF-2K, suggesting that inhibition of eEF-2K by tephrsoin could be a critical role in the potentiating effect of TSN on the cytotoxicity of 2-DG. Furthermore, we showed that the blunted autophagy and enhanced cytotoxicity of 2-DG was accompanied by the augmentation of apoptosis. These results show that TSN may be valuable for augmenting the therapeutic efficacy of 2-DG.
