Ophiopogonin DCAS# 41753-55-3 |
- OJV-VI
Catalog No.:BCX0611
CAS No.:125150-67-6
Quality Control & MSDS
3D structure
Package In Stock
Number of papers citing our products
| Cas No. | 41753-55-3 | SDF | Download SDF |
| PubChem ID | 46173859 | Appearance | White powder |
| Formula | C44H70O16 | M.Wt | 855.02 |
| Type of Compound | Steroids | Storage | Desiccate at -20°C |
| Synonyms | OJV-VI;945619-74-9;125150-67-6;Deacetylophiopogonin C | ||
| Solubility | Soluble in methan | ||
| Chemical Name | (2S,3R,4R,5R,6S)-2-[(2R,3R,4S,5S,6R)-5-hydroxy-2-[(1S,2S,4S,5'R,6R,7S,8R,9S,12S,13R,14R,16R)-16-hydroxy-5',7,9,13-tetramethylspiro[5-oxapentacyclo[10.8.0.02,9.04,8.013,18]icos-18-ene-6,2'-oxane]-14-yl]oxy-6-methyl-4-[(2S,3R,4S,5R)-3,4,5-trihydroxyoxan-2-yl]oxyoxan-3-yl]oxy-6-methyloxane-3,4,5-triol | ||
| SMILES | CC1CCC2(C(C3C(O2)CC4C3(CCC5C4CC=C6C5(C(CC(C6)O)OC7C(C(C(C(O7)C)O)OC8C(C(C(CO8)O)O)O)OC9C(C(C(C(O9)C)O)O)O)C)C)C)OC1 | ||
| Standard InChIKey | FHKHGNFKBPFJCB-LYLKFOBISA-N | ||
| Standard InChI | InChI=1S/C44H70O16/c1-18-9-12-44(54-16-18)19(2)30-28(60-44)15-26-24-8-7-22-13-23(45)14-29(43(22,6)25(24)10-11-42(26,30)5)57-41-38(59-40-36(52)34(50)31(47)20(3)55-40)37(32(48)21(4)56-41)58-39-35(51)33(49)27(46)17-53-39/h7,18-21,23-41,45-52H,8-17H2,1-6H3/t18-,19+,20+,21-,23-,24-,25+,26+,27-,28+,29-,30+,31+,32+,33+,34-,35-,36-,37+,38-,39+,40+,41+,42+,43+,44-/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. |
||
| 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. |
||
| 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 D plays a protective role as an effective antioxidant in H2O2-induced endothelial injury, it can be therefore developed as a novel drug for the therapy of cardiovascular disorders. 2. Ophiopogonin D can attenuate doxorubicin-induced autophagic cell death by relieving mitochondrial damage in vitro and in vivo. 3. Ophiopogonin D and spicatoside A can increase mucin production and secretion, by directly acting on airway epithelial cells, they could be as expectorants in diverse inflammatory pulmonary diseases. 4. Ophiopogonin D inhibits MCF-7 cell growth via the induction of cell cycle arrest at the G2/M phase. |
| Targets | MMP(e.g.TIMP) | p38MAPK | ROS | Caspase |
Ophiopogonin D Dilution Calculator
Ophiopogonin D Molarity Calculator
| 1 mg | 5 mg | 10 mg | 20 mg | 25 mg | |
| 1 mM | 1.1696 mL | 5.8478 mL | 11.6956 mL | 23.3913 mL | 29.2391 mL |
| 5 mM | 0.2339 mL | 1.1696 mL | 2.3391 mL | 4.6783 mL | 5.8478 mL |
| 10 mM | 0.117 mL | 0.5848 mL | 1.1696 mL | 2.3391 mL | 2.9239 mL |
| 50 mM | 0.0234 mL | 0.117 mL | 0.2339 mL | 0.4678 mL | 0.5848 mL |
| 100 mM | 0.0117 mL | 0.0585 mL | 0.117 mL | 0.2339 mL | 0.2924 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. | |||||
Calcutta University
University of Minnesota
University of Maryland School of Medicine
University of Illinois at Chicago
The Ohio State University
University of Zurich
Harvard University
Colorado State University
Auburn University
Yale University
Worcester Polytechnic Institute
Washington State University
Stanford University
University of Leipzig
Universidade da Beira Interior
The Institute of Cancer Research
Heidelberg University
University of Amsterdam
University of Auckland
TsingHua University
The University of Michigan
Miami University
DRURY University
Jilin University
Fudan University
Wuhan University
Sun Yat-sen University
Universite de Paris
Deemed University
Auckland University
The University of Tokyo
Korea University
- Ginsenoside Rb1
Catalog No.:BCN1063
CAS No.:41753-43-9
- Acuminatin
Catalog No.:BCN5477
CAS No.:41744-39-2
- (-)-Sativan
Catalog No.:BCN7752
CAS No.:41743-86-6
- Irisflorentin
Catalog No.:BCN1278
CAS No.:41743-73-1
- Pyrochamissanthin
Catalog No.:BCN3612
CAS No.:41743-60-6
- Sugeroside
Catalog No.:BCN6961
CAS No.:41743-57-1
- Luteone
Catalog No.:BCN5476
CAS No.:41743-56-0
- Procyanidin A2
Catalog No.:BCN6805
CAS No.:41743-41-3
- Bavachromene
Catalog No.:BCN3191
CAS No.:41743-38-8
- Croalbidine
Catalog No.:BCN2068
CAS No.:41714-30-1
- Indicine N-oxide
Catalog No.:BCN1996
CAS No.:41708-76-3
- Epimagnolin A
Catalog No.:BCN7831
CAS No.:41689-51-4
- Dihydrophaseic acid
Catalog No.:BCN5478
CAS No.:41756-77-8
- Evonimine
Catalog No.:BCN3082
CAS No.:41758-69-4
- ar-Curcumene
Catalog No.:BCN7534
CAS No.:4176-06-1
- 14-Deoxyandrographolide
Catalog No.:BCN3706
CAS No.:4176-97-0
- Lenvatinib (E7080)
Catalog No.:BCC1172
CAS No.:417716-92-8
- H-Leu-pNA.HCl
Catalog No.:BCC2972
CAS No.:4178-93-2
- Hypecorinine
Catalog No.:BCN3298
CAS No.:41787-57-9
- Junicedric acid
Catalog No.:BCN7660
CAS No.:41787-69-3
- Hesperetin-7-methyl ether
Catalog No.:BCN8501
CAS No.:
- Mangiferolic acid
Catalog No.:BCN4636
CAS No.:4184-34-3
- Alatamine
Catalog No.:BCN3100
CAS No.:41855-33-8
- Bezafibrate
Catalog No.:BCC4639
CAS No.:41859-67-0
Ophiopogonin D attenuates doxorubicin-induced autophagic cell death by relieving mitochondrial damage in vitro and in vivo.[Pubmed:25378375]
J Pharmacol Exp Ther. 2015 Jan;352(1):166-74.
It has been reported that Ophiopogonin D (OP-D), a steroidal glycoside and an active component extracted from Ophiopogon japonicas, promotes antioxidative protection of the cardiovascular system. However, it is unknown whether OP-D exerts protective effects against doxorubicin (DOX)-induced autophagic cardiomyocyte injury. Here, we demonstrate that DOX induced excessive autophagy through the generation of reactive oxygen species (ROS) in H9c2 cells and in mouse hearts, which was indicated by a significant increase in the number of autophagic vacuoles, LC3-II/LC3-I ratio, and upregulation of the expression of GFP-LC3. Pretreatment with OP-D partially attenuated the above phenomena, similar to the effects of treatment with 3-methyladenine. In addition, OP-D treatment significantly relieved the disruption of the mitochondrial membrane potential by antioxidative effects through downregulating the expression of both phosphorylated c-Jun N-terminal kinase and extracellular signal-regulated kinase. The ability of OP-D to reduce the generation of ROS due to mitochondrial damage and, consequently, to inhibit autophagic activity partially accounts for its protective effects in the hearts against DOX-induced toxicity.
Ophiopogonin-D suppresses MDA-MB-435 cell adhesion and invasion by inhibiting matrix metalloproteinase-9.[Pubmed:25816153]
Mol Med Rep. 2015 Jul;12(1):1493-8.
Ophiopogonin-D is one of steroidal saponins isolated from the root of the Chinese medicinal plant Ophiopogon japonicas. It has been claimed to possess anti-inflammatory and anti-oxidant properties. The present study was the first to examine the anti-tumor metastasis properties of ophiopogonin-D. An MTT assay showed that ophiopogonin-D inhibited the proliferation of MDA-MB-435 melanoma cells, and decreased invasion was demonstrated using a Transwell invasion assay. Furthermore, adhesion of MDA-MB-435 cells to human umbilical vascular endothelial cells and to fibronectin was inhibited by ophiopogonin-D. Gelatin zymography and western blot analysis showed that ophiopogonin-D inhibited the expression and secretion of matrix metalloproteinase-9 (MMP-9), but not that of MMP-2. Inhibition of phosphorylation of p38 by ophiopogonin-D indicated its inhibition of the mitogen-activated protein kinase pathway. Overall, the results suggested that ophiopogonin-D may be considered as a candidate drug for treating or preventing tumor metastasis.
Effects of ophiopogonin D and spicatoside A derived from Liriope Tuber on secretion and production of mucin from airway epithelial cells.[Pubmed:24060215]
Phytomedicine. 2014 Jan 15;21(2):172-6.
In the present study, we investigated whether aqueous extract of Liriope Tuber, Ophiopogonin D and spicatoside A derived from Liriope Tuber affect basal or phorbol ester (phorbol 12-myristate 13-acetate, PMA)-induced airway mucin production and secretion from airway epithelial cells. Confluent NCI-H292 cells were treated with each agent for 24 h (basal production) or pretreated with each agent for 30 min and then stimulated with PMA for 24 h (PMA-induced production and secretion), respectively. MUC5AC airway mucin production and secretion were measured by ELISA. The results were as follows: (1) aqueous extract of Liriope Tuber stimulated basal mucin production and did not inhibit but increased PMA-induced mucin production; (2) Ophiopogonin D and spicatoside A stimulated basal mucin production and did not inhibit but increased PMA-induced mucin production; (3) two compounds increased PMA-induced mucin secretion. These results suggest that Ophiopogonin D and spicatoside A can increase mucin production and secretion, by directly acting on airway epithelial cells and, at least in part, explain the traditional use of aqueous extract of Liriope Tuber as expectorants in diverse inflammatory pulmonary diseases.
Ophiopogonin D inhibits cell proliferation, causes cell cycle arrest at G2/M, and induces apoptosis in human breast carcinoma MCF-7 cells.[Pubmed:26778229]
J Integr Med. 2016 Jan;14(1):51-9.
OBJECTIVE: To investigate the effects of Ophiopogonin D on human breast cancer MCF-7 cells. METHODS: Cell viability was assessed by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide and colony formation experiments. Cell cycle was measured with cell cycle flow cytometry and a living cell assay. Apoptosis and terminal deoxynucleoitidyl transferase-mediated dUTP nick end labeling assays were performed to detect the apoptosis of MCF-7 cells induced by Ophiopogonin D. Finally, Western blotting was used to explore the mechanism. RESULTS: Exposure of cells to Ophiopogonin D resulted in marked decreases in viable cells and colony formation with a dose-dependent manner. Treatment of these cells with Ophiopogonin D also resulted in cell cycle arrest at the G(2)/M phase, and increased apoptosis. Mechanistically, Ophiopogonin D-induced G(2)/M cell cycle arrest was associated with down-regulation of cyclin B1. Furthermore, activation of caspase-8 and caspase-9 was involved in Ophiopogonin D-induced apoptosis. CONCLUSION: The data suggested that Ophiopogonin D inhibits MCF-7 cell growth via the induction of cell cycle arrest at the G(2)/M phase.
[Ophiopogonin D protects cardiomyocytes against doxorubicin-induced injury through suppressing endoplasmic reticulum stress].[Pubmed:25322552]
Yao Xue Xue Bao. 2014 Aug;49(8):1117-23.
This study aimed to examine whether Ophiopogonin D (OP-D) is capable of protecting cardiomyocytes against DOX-induced injury and the mechanisms involved. H9c2 cells were cultured. MTT assay was used to evaluate cell viability and toxicity. Mito-tracker as fluorescence probe was used to measure ROS content raised from mitochondria. The mRNA and protein expression of ATF6alpha, GRP78 and CHOP were analyzed using real-time PCR and Western blotting, respectively. The results showed that a significant endoplasmic reticulum stress (ERS) was induced upon exposure of H9c2 cells to DOX as indicated by the increase in the expression of ERS related proteins, which was paralleled with the accumulation of reactive oxygen species (ROS) and decrease in the viability of H9c2 cells. Whereas, DOX-induced ROS accumulation and up-regulation of ERS related proteins were partially abolished by pretreatment with OP-D. Consequently, a DOX-induced ERS was mitigated by application of OP-D. Similarly, DOX-induced decrease in cell viability was partially attenuated by either inhibiting CHOP or pretreatment with N-acetylcysteine (NAC), an antioxidant. Moreover, cardiac ultrastructural abnormalities seen in mouse receiving DOX injections were obviously ameliorated by pretreatment of OP-D. Taken together, the present study proved that OP-D protects cardiomyocytes against DOX-induced injury, at least in part, through reducing ROS accumulation and alleviating ERS.
A metabonomic study of cardioprotection of ginsenosides, schizandrin, and ophiopogonin D against acute myocardial infarction in rats.[Pubmed:25249156]
BMC Complement Altern Med. 2014 Sep 23;14:350.
BACKGROUND: Metabonomics is a useful tool for studying mechanisms of drug treatment using systematic metabolite profiles. Ginsenosides Rg1 and Rb1, Ophiopogonin D, and schizandrin are the main bioactive components of a traditional Chinese formula (Sheng-Mai San) widely used for the treatment of coronary heart disease. It remains unknown the effect of individual bioactive component and how the multi-components in combination affect the treating acute myocardial infarction (AMI). METHODS: Rats were divided into 7 groups and dosed consecutively for 7 days with mono and combined-therapy administrations. Serum samples were analyzed by proton nuclear magnetic resonance (1H NMR) spectroscopy. Partial least squares discriminate analysis (PLS-DA) was employed to distinguish the metabolic profile of rats in different groups and identify potential biomarkers. RESULTS: Score plots of PLS-DA exhibited that combined-therapy groups were significantly different from AMI group, whereas no differences were observed for mono-therapy groups. We found that AMI caused comprehensive metabolic changes involving stimulation of glycolysis, suppression of fatty acid oxidation, together with disturbed metabolism of arachidonic acid, linoleate, leukotriene, glycerophospholipid, phosphatidylinositol phosphate, and some amino acids. beta-hydroxybutyrate, cholines and glucose were regulated by mono-therapy of schizandrin and ginsenosides respectively. Besides these metabolites, combined-therapy ameliorated more of the AMI-induced metabolic changes including glycerol, and O-acetyl glycoprotein. A remarkable reduction of lactate suggested the therapeutic effect of combined-therapy through improving myocardial energy metabolism. CONCLUSIONS: This study provided novel metabonomic insights on the mechanism of synergistic cardioprotection of combined-therapy with ginsenosides, schizandrin, and Ophiopogonin D, and demonstrated the potential of discovering new drugs by combining bioactive components from traditional Chinese formula.
