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|Source:||The roots of Panax ginseng C. A. Mey.|
|1. 20S-protopanaxdiol saponins (PQDS) injection can obviously improve the ECG in Pit-induced AMI rats, alleviate the degree of cardiamyopathy in Iso-induced AMI rats, may via effect on AMI and anti-lipid peroxidation.
2. PQDS estrain the release of antistreptokinase (ASK), CK and lactate dehydrogenase (LDH), increase the activity of SOD and decrease the content of MDA.
3. PQDS has the effect of anti-tumor through increasing the activity of body immunity,improving the lymphocyte transformation,the activity of NK cells and the contents of IL-2 significantly.
|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).
Whenever 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||2.1739 mL||10.8696 mL||21.7391 mL||43.4783 mL||54.3478 mL|
|5 mM||0.4348 mL||2.1739 mL||4.3478 mL||8.6957 mL||10.8696 mL|
|10 mM||0.2174 mL||1.087 mL||2.1739 mL||4.3478 mL||5.4348 mL|
|50 mM||0.0435 mL||0.2174 mL||0.4348 mL||0.8696 mL||1.087 mL|
|100 mM||0.0217 mL||0.1087 mL||0.2174 mL||0.4348 mL||0.5435 mL|
Chirality. 2015 Feb;27(2):170-6. doi: 10.1002/chir.22407.
|Stereoselective formation and metabolism of 20(S)-protopanaxadiol ocotillol type epimers in vivo and in vitro.[Pubmed: 25422175]|
|(20S,24S)-epoxy-dammarane-3,12,25-triol (24S-epimer) and (20S,24R)-epoxy- dammarane-3,12,25-triol (24R-epimer), a pair of ocotillol type epimers, were identified as the main metabolites of (20S)-Protopanaxdiol (PPD). The aim of this study was to systematically investigate the formation and metabolism of this pair of epimers in vivo and in vitro and to elucidate the isoforms of cytochrome P450 enzymes responsible for the stereoselective metabolism of both epimers. The result showed that 24S-epimer was a more predominant ingredient in rat plasma after oral administration of (20S)-Protopanaxdiol with higher area under the curve (AUC) values. Both the enzyme kinetic evaluations of the formation and elimination of 24S-epimer and 24R-epimer in rat liver microsomes (RLM) and human liver microsomes (HLM) indicated that 24S-epimer had a higher formation rate and a lower oxygenation metabolism rate than 24R-epimer, and the stereoselective differences were more obvious in HLM than in RLM. The chemical inhibition and recombinant human P450 isoforms assay showed that CYP3A4 was the predominant isoform responsible for the further metabolism of 24R-epimer in HLM. The biliary excretion ratio of the 24S-epimer glucuronide was more than 28-fold higher than that of 24R-epimer glucuronide after intravenous administration to rats, which also indicated 24S-epimer was more preferential to be metabolized as the glucuronide conjugate than 24R-epimer.|
PLoS One. 2014 Jun 2;9(6):e98887.
|Stereoselective property of 20(S)-protopanaxadiol ocotillol type epimers affects its absorption and also the inhibition of P-glycoprotein.[Pubmed: 24887182]|
|Stereoselectivity has been proved to be tightly related to drug action including pharmacodynamics and pharmacokinetics. (20S,24R)-epoxy-dammarane-3,12,25-triol (24R-epimer) and (20S,24S)-epoxy-dammarane-3,12,25-triol (24S-epimer), a pair of (20S)-Protopanaxdiol(PPD) ocotillol type epimers, were the main metabolites of (20S)-Protopanaxdiol. Previous studies have shown that 24R-epimer and 24S-epimer had stereoselectivity in pharmacological action and pharmacokinetics. In the present study, the aim was to further study the pharmacokinetic characteristics of both epimers, investigate their absorption mechanism and analyze the selectivity effects of ocotillol type side chain and C24 stereo-configuration on P-glycoprotein (P-gp) in vivo and in vitro. Results showed that the absolute bioavailability of 24R-epimer was about 14-fold higher than that of 24S-epimer, and a linear kinetic characteristic was acquired in doses of 5-20 mg/kg for both epimers after oral administration. Furthermore, the apparent permeability coefficients of 24R-epimer were 5-7 folds higher than that of 24S-epimer having lower efflux ratios in Caco-2 cell models. Moreover, both 24R-epimer and 24S-epimer had similar inhibitory effects on P-gp by increasing cellular retention of rhodamine 123 in Caco-2 cells and decreasing efflux of digoxin across Caco-2 cell monolayers. In situ in vivo experiments showed that the inhibition of 24R-epimer on P-gp was stronger than that of 24S-epimer by single-pass intestinal perfusion of rhodamine 123 in rats. Western blot analyses demonstrated that both epimers had no action on P-gp expression in Caco-2 cells. In conclusion, with respect to the stereoselectivity, C24 S-configuration of the ocotillol type epimers processed a poor transmembrane permeability and could be distinguished by P-gp. Sharing a dammarane skeleton, both 24R-epimer and 24S-epimer were potent inhibitors of P-gp. This study provides a new case of stereoselective pharmacokinetics of chiral compounds which contributes to know the chiral characteristics of P-gp and structure-action relationship of (20S)-Protopanaxdiol type and ocotillol type ginsenosides as a P-gp inhibitor.|
Drug Metab Dispos. 2011 Mar;39(3):472-83.
|Identification of 20(S)-protopanaxadiol metabolites in human liver microsomes and human hepatocytes.[Pubmed: 21139039]|
|(20S)-Protopanaxdiol (PPD, 1) is one of the aglycones of the ginsenosides and has a wide range of pharmacological activities. At present, (20S)-Protopanaxdiol has progressed to early clinical trials as an antidepressant. In this study, its fate in mixed human liver microsomes (HLMs) and human hepatocytes was examined for the first time. By using liquid chromatography-electrospray ionization ion trap mass spectrometry, 24 metabolites were found. Four metabolites were isolated, and their structures were elucidated as (20S,24S)-epoxydammarane-3,12,25-triol (2), (20S,24R)-epoxydammarane-3,12,25-triol (3), (20S,24S)-epoxydammarane-12,25-diol-3-one (4), and (20S,24R)-epoxydammarane-12,25-diol-3-one (5) based on a detailed analysis of their spectroscopic data. The predominant metabolic pathway of PPD observed was the oxidation of the 24,25-double bond to yield 24,25-epoxides, followed by hydrolysis and rearrangement to form the corresponding 24,25-vicinal diol derivatives (M6) and the 20,24-oxide form (2 and 3). Further sequential metabolites (M2-M5) were also detected through the hydroxylation and dehydrogenation of 2 and 3. All of the phase I metabolites except for M1-1 possess a hydroxyl group at C-25 of the side chain, which was newly formed by biotransformation. Two glucuronide conjugates (M7) attributed to 2 and 3 were detected in human hepatocyte incubations, and their conjugation sites were tentatively assigned to the 25-hydroxyl group. The findings of this study strongly suggested that the formation of the 25-hydroxyl group is very important for the elimination of (20S)-Protopanaxdiol.|
Planta Med. 2009 Aug;75(10):1124-8.
|20S-protopanaxadiol inhibits P-glycoprotein in multidrug resistant cancer cells.[Pubmed: 19291609]|
|One of the major causes for cancer cells to resist current chemotherapy is attributed to the over-expression of P-glycoprotein (P-gp), resulting in insufficient drug delivery to the tumor sites. Protopanaxadiol ginsenosides Rg3 and Rh2 are known to induce apoptosis and significantly enhance the tumor inhibitory effects of chemotherapeutics in a synergistic fashion. One of the possible mechanisms is by blocking P-gp activity. The final deglycosylation metabolite of protopanaxadiols (PPDs) IN VIVO is (20S)-Protopanaxdiol (aglycone PPD, aPPD), which has also shown anticancer activity and synergy with chemotherapy drugs. In the present study, P-gp over-expressing cancer cells were utilized to test whether (20S)-Protopanaxdiol also inhibits P-gp activity. We found that (20S)-Protopanaxdiol caused similar cytotoxicity in P388adr cells as their parental non-MDR cells, suggesting that (20S)-Protopanaxdiol may not be a substrate of P-gp. On the other hand, the calcein AM efflux assay showed that (20S)-Protopanaxdiol was able to inhibit P-gp activity as potently as verapamil on MDR cells. The blockage of P-gp activity was highly reversible as wash-out of (20S)-Protopanaxdiol resulted in an immediate recovery of P-gp activity. Unlike verapamil, (20S)-Protopanaxdiol did not affect ATPase activity of P-gp suggesting a different mechanism of action. The above results indicate that (20S)-Protopanaxdiol , unlike its precursor ginsenosides Rg3 and Rh2, is not a substrate of P-gp. It is also the first time that (20S)-Protopanaxdiol has showed a reversible nature of its P-gp inhibition. In addition to its pro-apoptotic nature, (20S)-Protopanaxdiol may be a potential new P-gp inhibitor for cancer treatment.|