Ginsenoside F2CAS# 62025-49-4 |
Quality Control & MSDS
Number of papers citing our products
Chemical structure
3D structure
| Cas No. | 62025-49-4 | SDF | Download SDF |
| PubChem ID | 9918692 | Appearance | White powder |
| Formula | C42H72O13 | M.Wt | 785.01 |
| Type of Compound | Triterpenoids | Storage | Desiccate at -20°C |
| Solubility | Soluble in Chloroform,Dichloromethane,Ethyl Acetate,DMSO,Acetone,etc. | ||
| Chemical Name | (2R,3S,4S,5R,6R)-2-(hydroxymethyl)-6-[[(3S,5R,8R,9R,10R,12R,13R,14R,17S)-12-hydroxy-4,4,8,10,14-pentamethyl-17-[(2S)-6-methyl-2-[(2S,3R,4S,5S,6R)-3,4,5-trihydroxy-6-(hydroxymethyl)oxan-2-yl]oxyhept-5-en-2-yl]-2,3,5,6,7,9,11,12,13,15,16,17-dodecahydro-1H-cyclopenta[a]phenanthren-3-yl]oxy]oxane-3,4,5-triol | ||
| SMILES | CC(=CCCC(C)(C1CCC2(C1C(CC3C2(CCC4C3(CCC(C4(C)C)OC5C(C(C(C(O5)CO)O)O)O)C)C)O)C)OC6C(C(C(C(O6)CO)O)O)O)C | ||
| Standard InChIKey | SWIROVJVGRGSPO-JBVRGBGGSA-N | ||
| Standard InChI | InChI=1S/C42H72O13/c1-21(2)10-9-14-42(8,55-37-35(51)33(49)31(47)25(20-44)53-37)22-11-16-41(7)29(22)23(45)18-27-39(5)15-13-28(38(3,4)26(39)12-17-40(27,41)6)54-36-34(50)32(48)30(46)24(19-43)52-36/h10,22-37,43-51H,9,11-20H2,1-8H3/t22-,23+,24+,25+,26-,27+,28-,29-,30+,31+,32-,33-,34+,35+,36-,37-,39-,40+,41+,42-/m0/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 | Ginsenoside F2, an autophagic initiater, which has anti-cancer, and anti-obesity activities. Ginsenoside F2 inhibited the growth and invasion of cancer, and activated the intrinsic apoptotic pathway and mitochondrial dysfunction. Ginsenoside F2 suppresses hair cell apoptosis and premature entry to catagen more effectively than finasteride, it decreases the expression of TGF-β2 and SCAP proteins, the factors in the SCAP pathway could be targets for hair loss prevention drugs. |
| Targets | PPAR | TGF-β/Smad | Wnt/β-catenin | Caspase | MMP(e.g.TIMP) |
| In vitro | Anti-Cancer Effect of Ginsenoside F2 against Glioblastoma Multiforme in Xenograft Model in SD Rats[Pubmed: 23717108]J Ginseng Res. 2012 Jan; 36(1): 86–92.The glioblastoma multiforme (GBM) is the most common malignant brain tumor in adults. Despite combination treatments of radiation and chemotherapy, the survival periods are very short.
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| In vivo | The inductive effect of ginsenoside F2 on hair growth by altering the WNT signal pathway in telogen mouse skin.[Pubmed: 24613976]Eur J Pharmacol. 2014 May 5;730:82-9.This study was conducted to confirm the possibility of using minor ginseng saponin F2 by oral administration on hair anagen induction effects.
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| Kinase Assay | Ginsenoside F2 induces apoptosis accompanied by protective autophagy in breast cancer stem cells.[Pubmed: 22326284]Cancer Lett. 2012 Aug 28;321(2):144-53.Ginsenoside F2 (F2) was assessed for its antiproliferative activity against breast cancer stem cells (CSCs).
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| Cell Research | Ginsenoside F2 possesses anti-obesity activity via binding with PPARγ and inhibiting adipocyte differentiation in the 3T3-L1 cell line.[Pubmed: 24666293]J Enzyme Inhib Med Chem. 2015 Feb;30(1):9-14.Panax ginseng Meyer has been shown to be effective in mitigating various diseases. Protopanaxadiols (PPD) and protopanaxatriols (PPT), which are the main constituents of ginseng, have been shown to impact obesity.
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Ginsenoside F2 Dilution Calculator
Ginsenoside F2 Molarity Calculator
| 1 mg | 5 mg | 10 mg | 20 mg | 25 mg | |
| 1 mM | 1.2739 mL | 6.3693 mL | 12.7387 mL | 25.4774 mL | 31.8467 mL |
| 5 mM | 0.2548 mL | 1.2739 mL | 2.5477 mL | 5.0955 mL | 6.3693 mL |
| 10 mM | 0.1274 mL | 0.6369 mL | 1.2739 mL | 2.5477 mL | 3.1847 mL |
| 50 mM | 0.0255 mL | 0.1274 mL | 0.2548 mL | 0.5095 mL | 0.6369 mL |
| 100 mM | 0.0127 mL | 0.0637 mL | 0.1274 mL | 0.2548 mL | 0.3185 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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Ginsenoside F2 induces apoptosis accompanied by protective autophagy in breast cancer stem cells.[Pubmed:22326284]
Cancer Lett. 2012 Aug 28;321(2):144-53.
Ginsenoside F2 (F2) was assessed for its antiproliferative activity against breast cancer stem cells (CSCs). F2 induced apoptosis in breast CSCs by activating the intrinsic apoptotic pathway and mitochondrial dysfunction. Concomitantly, F2 induced the formation of acidic vesicular organelles, recruitment of GFP-LC3-II to autophagosomes, and elevation of Atg-7 levels, suggesting that F2 initiates an autophagic progression in breast CSCs. Treatment with an inhibitor of autophagy enhanced F2-induced cell death. Our findings provide new insights into the anti-cancer activity of F2 and may contribute to the rational use and pharmacological study of F2.
Anti-Cancer Effect of Ginsenoside F2 against Glioblastoma Multiforme in Xenograft Model in SD Rats.[Pubmed:23717108]
J Ginseng Res. 2012 Jan;36(1):86-92.
The glioblastoma multiforme (GBM) is the most common malignant brain tumor in adults. Despite combination treatments of radiation and chemotherapy, the survival periods are very short. Therefore, this study was conducted to assess the potential of Ginsenoside F2 (F2) to treat GBM. In in vitro experiments with glioblastoma cells U373MG, F2 showed the cytotoxic effect with IC50 of 50 mug/mL through apoptosis, confirmed by DNA condensation and fragmentation. The cell population of cell cycle sub-G1 as indicative of apoptosis was also increased. In xenograft model in SD rats, F2 at dosage of 35 mg/kg weight was intravenously injected every two days. This reduced the tumor growth in magnetic resonance imaging images. The immunohistochemistry revealed that the anticancer activity might be mediated through inhibition of proliferation judged by Ki67 and apoptosis induced by activation of caspase-3 and -8. And the lowered expression of CD31 showed the reduction in blood vessel densities. The expression of matrix metalloproteinase-9 for invasion of cancer was also inhibited. The cell populations with cancer stem cell markers of CD133 and nestin were reduced. The results of this study suggested that F2 could be a new potential chemotherapeutic drug for GBM treatment by inhibiting the growth and invasion of cancer.
Ginsenoside F2 possesses anti-obesity activity via binding with PPARgamma and inhibiting adipocyte differentiation in the 3T3-L1 cell line.[Pubmed:24666293]
J Enzyme Inhib Med Chem. 2015 Feb;30(1):9-14.
Abstract Panax ginseng Meyer has been shown to be effective in mitigating various diseases. Protopanaxadiols (PPD) and protopanaxatriols (PPT), which are the main constituents of ginseng, have been shown to impact obesity. Therefore, we selected several important ginsenosides to perform our docking study and determine if they had binding affinity with the peroxisome proliferator activated receptor gamma (PPARgamma), which is a major transcription factor in adipocytes. Among them, only a few ginsenosides demonstrated binding affinity with PPARgamma. Other than Ginsenoside F2 rest of them were previously reported by the researchers in experimental study in case of obesity cell line 3T3-L1 adipocyte. In few recent studies, it was reported that F2 has protective effects on malignant brain tumors as well as anti-cancer activity in breast cancer. Therefore, we felt it was important to focus on F2 when considering obesity. Our study focused on this ginsenoside and analyzed its impact on 3T3-L1 adipocytes. Following the molecular interaction studies, further experimental studies were carried out and demonstrated that Ginsenoside F2 when treated with different doses reduces the level of lipid accumulated by the 3T3-L1 cell line during adipogenesis. Reverse transcriptase polymerase chain reaction (RT-PCR) and quantitative real-time PCR results showed reduction in PPARgamma and perilipin gene expression levels compared to that of differentiated adipocytes without any treatment. So considering the binding with a major adipocyte transcription factor and the performed experiments, we suggest that Ginsenoside F2 may reduce obesity via the inhibition of adipogenesis in the 3T3-L1 cell line.
The inductive effect of ginsenoside F2 on hair growth by altering the WNT signal pathway in telogen mouse skin.[Pubmed:24613976]
Eur J Pharmacol. 2014 May 5;730:82-9.
This study was conducted to confirm the possibility of using minor ginseng saponin F2 by oral administration on hair anagen induction effects. The signaling pathway and anagen induction effect of Ginsenoside F2 were investigated and compared with finasteride on the effect of hair growth induction. The cell-based MTT assay results indicated that the proliferation rates of HHDPC and HaCaT treated with F2 significantly increased by 30% compared with the finasteride-treated group. A western blot study showed that the expression of beta-catenin Lef-1 and DKK-1 increased by 140, 200% and decreased by 40% in the F2-treated group, respectively compared to that of finasteride-treated group. C57BL/6 mice were subjected to the same treatments. The hair growth promotion rates were compared with groups treated with finasteride, which was 20% higher in the F2-treated group. Tissue histological analysis results showed the number of hair follicles, thickness of the epidermis, and follicles of the anagen phase which increased in the F2-treated group, compared with the finasteride-treated groups. Moreover, the effect of F2 on hair growth was confirmed through the immunofluorescence (IF) methods indicating the expression aspect of Wnt signal pathway-related factors in the tissue of C57BL/6 mouse. Our results considered the expression increase in beta-catenin, Lef-1 which was suggested as a major factor related to the development and growth of hair follicle and the decrease in DKK-1 when entering catagen by F2. As the data showed, F2 might be a potential new therapeutic source for anagen induction and hair growth through the Wnt signal pathway.
Ginsenoside F2 reduces hair loss by controlling apoptosis through the sterol regulatory element-binding protein cleavage activating protein and transforming growth factor-beta pathways in a dihydrotestosterone-induced mouse model.[Pubmed:24789999]
Biol Pharm Bull. 2014;37(5):755-63.
This study was conducted to test whether Ginsenoside F2 can reduce hair loss by influencing sterol regulatory element-binding protein (SREBP) cleavage-activating protein (SCAP) and the transforming growth factor beta (TGF-beta) pathway of apoptosis in dihydrotestosterone (DHT)-treated hair cells and in a DHT-induced hair loss model in mice. Results for Ginsenoside F2 were compared with finasteride. DHT inhibits proliferation of hair cells and induces androgenetic alopecia and was shown to activate an apoptosis signal pathway both in vitro and in vivo. The cell-based 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay showed that the proliferation rates of DHT-treated human hair dermal papilla cells (HHDPCs) and HaCaTs increased by 48% in the Ginsenoside F2-treated group and by 12% in the finasteride-treated group. Western blot analysis showed that Ginsenoside F2 decreased expression of TGF-beta2 related factors involved in hair loss. The present study suggested a hair loss related pathway by changing SCAP related apoptosis pathway, which has been known to control cholesterol metabolism. SCAP, sterol regulatory element-binding protein (SREBP) and caspase-12 expression in the Ginsenoside F2-treated group were decreased compared to the DHT and finasteride-treated group. C57BL/6 mice were also prepared by injection with DHT and then treated with Ginsenoside F2 or finasteride. Hair growth rate, density, thickness measurements and tissue histotological analysis in these groups suggested that Ginsenoside F2 suppressed hair cell apoptosis and premature entry to catagen more effectively than finasteride. Our results indicated that Ginsenoside F2 decreased the expression of TGF-beta2 and SCAP proteins, which have been suggested to be involved in apoptosis and entry into catagen. This study provides evidence those factors in the SCAP pathway could be targets for hair loss prevention drugs.
