Ophiopogonin BCAS# 38971-41-4 |
Quality Control & MSDS
Number of papers citing our products
Chemical structure
3D structure
| Cas No. | 38971-41-4 | SDF | Download SDF |
| PubChem ID | 3081483 | Appearance | Powder |
| Formula | C39H62O12 | M.Wt | 722.91 |
| Type of Compound | Steroids | Storage | Desiccate at -20°C |
| Solubility | Soluble in Chloroform,Dichloromethane,Ethyl Acetate,DMSO,Acetone,etc. | ||
| SMILES | CC1CCC2(C(C3C(O2)CC4C3(CCC5C4CC=C6C5(C(CC(C6)O)OC7C(C(C(C(O7)C)O)O)OC8C(C(C(C(O8)C)O)O)O)C)C)C)OC1 | ||
| Standard InChIKey | OWGURJWJHWYCIQ-ALQLZCPRSA-N | ||
| Standard InChI | InChI=1S/C39H62O12/c1-17-9-12-39(46-16-17)18(2)28-26(51-39)15-25-23-8-7-21-13-22(40)14-27(38(21,6)24(23)10-11-37(25,28)5)49-36-34(32(44)30(42)20(4)48-36)50-35-33(45)31(43)29(41)19(3)47-35/h7,17-20,22-36,40-45H,8-16H2,1-6H3/t17-,18+,19+,20-,22-,23-,24+,25?,26+,27-,28+,29+,30-,31-,32+,33-,34-,35+,36+,37+,38+,39-/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. Ophiopogonin B is often used in Chinese traditional medicine to treat pulmonary disease, it is a prospective inhibitor of PI3K/Akt and may be used as an alternative compound to treat NSCLC. 2. Ophiopogonin B induces apoptosis, mitotic catastrophe and autophagy , has inhibitory effect on adhesion, invasion and migration of A549 cells in vitro. 3. Ophiopogonin B may be considered a potential inhibitor of gastric cancer progression, and may be used as an alternative compound for its treatment. |
| Targets | Caspase | PI3K | Akt | mTOR | ROS | ERK | JNK | Bcl-2/Bax | MMP(e.g.TIMP) |
Ophiopogonin B Dilution Calculator
Ophiopogonin B Molarity Calculator
| 1 mg | 5 mg | 10 mg | 20 mg | 25 mg | |
| 1 mM | 1.3833 mL | 6.9165 mL | 13.833 mL | 27.666 mL | 34.5825 mL |
| 5 mM | 0.2767 mL | 1.3833 mL | 2.7666 mL | 5.5332 mL | 6.9165 mL |
| 10 mM | 0.1383 mL | 0.6916 mL | 1.3833 mL | 2.7666 mL | 3.4582 mL |
| 50 mM | 0.0277 mL | 0.1383 mL | 0.2767 mL | 0.5533 mL | 0.6916 mL |
| 100 mM | 0.0138 mL | 0.0692 mL | 0.1383 mL | 0.2767 mL | 0.3458 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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Ophiopogonin B-induced autophagy in non-small cell lung cancer cells via inhibition of the PI3K/Akt signaling pathway.[Pubmed:23151908]
Oncol Rep. 2013 Feb;29(2):430-6.
Ophiopogonin B (OP-B) is a bioactive component of Radix Ophiopogon Japonicus, which is often used in Chinese traditional medicine to treat pulmonary disease. However, whether or not OP-B has any potential antitumor activity has not been reported. Here, we show that the non-small cell lung cancer (NSCLC) cell lines NCI-H157 and NCI-H460 treated with OP-B grow more slowly and accumulate vacuoles in their cytoplasm compared to untreated control cells. Flow cytometric analysis showed that the cells were arrested in G0/G1 phase. Nuclear morphology, Annexin-V/PI staining, and expression of cleaved caspase-3 all confirm that OP-B does not induce apoptosis. Instead, based on results from both transmission electron microscopy (TEM) and the expression of microtubule-associated protein 1 light chain 3-II (LC3-II), we determined that OP-B treatment induced autophagy in both cell lines. Next, we examined the PI3K/Akt/mTOR signaling pathway and found that OP-B inhibited phosphorylation of Akt (Ser473, Thr308) in NCI-H157 cells and also inhibited several key components of the pathway in NCI-H460 cells, such as p-Akt(Ser473, Thr308), p-p70S6K (Thr389). Additionally, insulin-mediated activation of the PI3K/Akt/mTOR pathway provides evidence that activation of this pathway may correlate with induction of autophagy in H460 cells. Therefore, OP-B is a prospective inhibitor of PI3K/Akt and may be used as an alternative compound to treat NSCLC.
Ophiopogonin B induces apoptosis, mitotic catastrophe and autophagy in A549 cells.[Pubmed:27175570]
Int J Oncol. 2016 Jul;49(1):316-24.
Ophiopogonin B (OP-B), a saponin compound isolated from Radix Ophiopogon japonicus, was verified to inhibit cell proliferation in numerous non-small cell lung cancer (NSCLC) cells in our previous study. However, the precise mechanisms of action have remained unclear. In the present study, we mainly investigated the effects of OP-B on adenocarcinoma A549 cells to further elaborate the underlying mechanisms of OP-B in different NSCLC cell lines. Detection by high content screening (HCS) and TUNEL assay verified that OP-B induced apoptosis in this cell line, while detection of Caspase-3, Bcl-2 and Bax showed that OP-B induced cell death was caspase and mitochondrial independent. Further experiments showed that OP-B induced cell cycle arrest in the S and G2/M phases by inhibiting the expression of Myt1 and phosphorylation of Histone H3 (Ser10), which resulted in mitotic catastrophe in the cells. Transmission electron microscopy (TEM) observation of cell micro-morphology combined with detection of Atgs by western blot analysis showed that OP-B induced autophagy in this cell line. Autophagy inhibition by the lysosome inhibitor CQ or Beclin1-siRNA knockdown both attenuated cell viability, demonstrated that autophagy also being the vital reason resulted in cell death. More importantly, the xenograft model using A549 cells provided further evidence of the inhibition of OP-B on tumor proliferation. Immunohistochemistry detection of LC3 and Tunel assay both verified that high dose of OP-B (75 mg/kg) induced autophagy and apoptosis in vivo, and western blot detection of p-Histone H3 (Ser10), Survivin and XIAP further indicated the molecular mechanism of OP-B in vivo. As our findings revealed, multiple types of cell death overlapped in OP-B treated A549 cells, it displayed multitarget characteristics of the compounds extracted from the Chinese herbal, which may be used as candidate anticancer medicine in clinic.
[Molecular mechanism of ophiopogonin B induced cellular autophagy of human cervical cancer HeLa cells].[Pubmed:23984518]
Yao Xue Xue Bao. 2013 Jun;48(6):855-9.
This study is to investigate the antitumor activity of Ophiopogonin B (OP-B). MTT assay, flow cytometric analysis, acridine orange staining, Lyso-Tracker Red staining and HeLa-GFP-LC3 transfect cells assay were used to detect the proliferation activity, apoptosis and autophagy of HeLa cells. The results showed that OP-B exerted potent antiproliferative activity on HeLa cells, the cell growth inhibition effect of OP-B was not due to apoptosis and OP-B could induce autophagy of HeLa cells. OP-B also induced the protein expression up-regulation of Beclin-1 and promoted LC3 I transformation LC3 II, which were representative proteins of autophagy. Furthermore, 3-MA, an inhibitor of autophagy, not only inhibited OP-B-mediated autophagy but also almost completely reversed the antiproliferative effect of OP-B, suggesting that the growth inhibition effect of OP-B was autophagy dependent. Western blotting demonstrated that OP-B inhibited the phosphorylation of Akt and its' downstream vital protein, such as mTOR and p70S6K. In addition, OP-B also induced the protein expression up-regulation of PTEN, which is a negative regulation protein for Akt/mTOR signaling pathway. However, OP-B did not affect the protein expression of total Akt. Collectively, the antitumor effects of OP-B were autophagy-dependent via repression Akt/mTOR signaling pathway. Therefore, OP-B is a prospective inhibitor of Akt/mTOR and may be used as an alternative compound to treat cervical carcinoma.
Effects of ophiopogonin B on the proliferation and apoptosis of SGC7901 human gastric cancer cells.[Pubmed:27121658]
Mol Med Rep. 2016 Jun;13(6):4981-6.
Ophiopogonin B (OPB) is a bioactive component of Radix Ophiopogon japonicus, which is often used in traditional Chinese medicine to treat cancer. The present study aimed to investigate the antitumor activity of OPB in gastric cancer. Cell Counting kit8, flow cytometry with Annexin Vfluorescein isothiocyanate, Hoechst staining, mitochondrial membrane potential (MMP) detection, and reactive oxygen species (ROS) assay were used to detect the biological function of SGC7901 gastric cancer cells. The results demonstrated that high concentrations of OPB (5, 10 and 20 micromol/l) exerted potent antiproliferative effects on SGC7901 cells in a dosedependent manner. Furthermore, apoptotic rates were increased and cell morphology was altered following treatment with OPB. In addition, OPBinduced apoptosis of SGC7901 cells was associated with loss of MMP and increased ROS generation. Western blotting indicated that treatment with OPB increased the protein expression levels of caspase3 and Bcell lymphoma 2 (Bcl2)associated X protein, whereas the expression levels of Bcl2 and the phosphorylation levels of extracellular signalregulated kinases 1/2 and cJun Nterminal kinases 1/2 were decreased. These results suggest that OPB may be considered a potential inhibitor of gastric cancer progression, and may be used as an alternative compound for its treatment.
