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Polyphyllin D
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Product Name Polyphyllin D
Price: $118 / 20mg
CAS No.: 50773-41-6
Catalog No.: CFN90255
Molecular Formula: C44H70O16
Molecular Weight: 855.02 g/mol
Purity: >=98%
Type of Compound: Steroids
Physical Desc.: Powder
Source: The rhizomes of Paris yunnanensis Franch.
Solvent: DMSO, Pyridine, Methanol, Ethanol, etc.
Download: COA    MSDS    SDF    Manual
Similar structural: Comparison (Web)  (SDF)
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Related Screening Libraries
Size /Price /Stock 10 mM * 100 uL in DMSO / Inquiry / In-stock
10 mM * 1 mL in DMSO / Inquiry / In-stock
Related Libraries
Biological Activity
Description: Polyphyllin D has anti-angiogenic, and anticancer effects, it induces apoptosis via the mitochondrial apoptotic pathway as evidenced by decreased Bcl-2 expression levels, disruption of MMP and increased Bax, cytochrome C and cleaved-caspase-3 levels.Polyphyllin D has toxicity in human RBCs as well as its underlying mechanism for the hemolysis and eryptosis/erythroptosis.
Targets: Bcl-2/Bax | Caspase | MMP(e.g.TIMP) | p21 | JNK | Calcium Channel | VEGFR | HIF
In vitro:
J Pharm Pharmacol. 2014 May;66(5):713-21.
Polyphyllin D induces apoptosis in K562/A02 cells through G2/M phase arrest.[Pubmed: 24325805]
The effect of Polyphyllin D on inducing cell death of the K562/A02 human leukaemia drug-resistant cells in vitro was examined.
METHODS AND RESULTS:
The effect of Polyphyllin D on K562/A02 cells were analysed by studying their cytotoxicity, apoptosis, cell cycle distribution, caspase-3 activity and disruption of mitochondrial membrane potential (MMP). Polyphyllin D, a small molecular monomer extracted from rhizoma of Paris polyphyllin, exhibited strong anticancer activity in a previous study. Our results demonstrate that Polyphyllin D exerts a growth inhibitory effect by arresting cells at G2/M phase and by the induction of apoptosis in K562/A02 human leukaemia drug-resistant cells, G2/M phase arrest was found to be associated with up-regulation of p21 and down-regulation of cyclin B1 and cyclin-dependent protein kinase 1. Polyphyllin D-induced apoptosis via the mitochondrial apoptotic pathway as evidenced by decreased Bcl-2 expression levels, disruption of MMP and increased Bax, cytochrome C and cleaved-caspase-3 levels.
CONCLUSIONS:
These data suggest that Polyphyllin D has a potential as a potent therapeutic agent for chronic myeloid leukaemia.
Arch Toxicol. 2012 May;86(5):741-52.
Polyphyllin D induces apoptosis in human erythrocytes through Ca²⁺ rise and membrane permeabilization.[Pubmed: 22349056]
Polyphyllin D (PD) is a potent anticancer agent isolated from a traditional medicinal herb Paris polyphylla that has been used in China for many years to treat cancer. Polyphyllin D is not a substrate of p-glycoprotein, and it can bypass the multi-drug resistance in cancer cell line R-HepG2. However, the effect of Polyphyllin D on the induction of cell death in human erythrocytes remains unknown. Given that Polyphyllin D is a small molecule that can depolarize the mitochondrial membrane potential and release apoptosis-inducing factor (AIF) in isolated mitochondria, we hypothesized that the apoptogenic effect of Polyphyllin D in human erythrocytes devoid of mitochondria would be minimal. This study therefore tried to evaluate the in vitro effect of Polyphyllin D on hemolysis and apoptosis in human erythrocytes.
METHODS AND RESULTS:
Apoptosis in human red blood cells (RBCs), also known as eryptosis or erythroptosis, after Polyphyllin D treatment was determined by flow cytometry and confocal microscopy for the phosphatidyl-serine externalization and other apoptosis feature events. False to our prediction, Polyphyllin D caused hemolysis and eryptosis/erythroptosis in human RBCs. Mechanistically, elevation in the cytosolic Ca²⁺ ion level seems to be a key but not the only mediator in the Polyphyllin D-mediated eryptosis/erythroptosis because depletion of the external Ca²⁺ could not eliminate the Polyphyllin D effect. Also, Polyphyllin D was able to permeabilize the membrane of RBC ghosts in a way similar to digitonin.
CONCLUSIONS:
Taken together, we report here for the first time the toxicity of Polyphyllin D in human RBCs as well as its underlying mechanism for the hemolysis and eryptosis/erythroptosis.
Acta Biochim Biophys Sin (Shanghai) . 2017 Jun 1;49(6):479-486.
Polyphyllin I induces G2/M phase arrest and apoptosis in U251 human glioma cells via mitochondrial dysfunction and the JNK signaling pathway[Pubmed: 28449039]
Abstract Glioblastoma is the most aggressive brain tumor, and its prognosis remains poor. Therefore, novel therapeutic strategies are needed for glioma therapy. Polyphyllin I (PPI), a bioactive constituent extracted from Paris polyphylla, was reported to have anti-tumor activity. However, the detailed mechanism for this activity remains unclear. Here, we investigated the inhibitory effects of PPI on glioma cells and its mechanisms in vitro. U251 cells were treated with various concentrations of PPI (2-9 μM) for 24 to 72 h. The inhibition of U251 cell proliferation by PPI was assessed by MTT assay. The effects on cell cycle and apoptosis were examined by flow cytometry with PI and annexin V-FITC/PI dual staining, and the cell mitochondrial membrane potential level was evaluated by fluorescence microscopy with JC-1 staining. The expression levels of apoptosis-related proteins and JNK signal pathway proteins were evaluated by western blot analysis. Results showed that PPI significantly inhibited the proliferation of U251 cells in a concentration-dependent manner. PPI induced G2/M phase arrest and apoptosis, and it upregulated the expressions of Bax, cytochrome c, and p-JNK, but downregulated the expression of the anti-apoptotic protein Bcl-2 in U251 cells. Moreover, PPI provoked the depolarization of the mitochondrial membrane potential. In addition, apoptosis induced by the PPI was remarkably suppressed by the JNK inhibitor SP600125. Our data provide evidence that PPI inhibits proliferation and induces apoptotic cell death in U251 cells. This effect may be associated with the JNK pathway. These results suggest that PPI is an activator of the JNK signaling pathway with a potential anti-glioma effect. Keywords: JNK pathway; U251 cell; apoptosis; cell cycle; polyphyllin I.
In vivo:
J Ethnopharmacol. 2011 Sep 1;137(1):64-9.
Polyphyllin D, a steroidal saponin from Paris polyphylla, inhibits endothelial cell functions in vitro and angiogenesis in zebrafish embryos in vivo.[Pubmed: 21658438]
Angiogenesis, the process of blood vessel formation, is critical to tumour growth. The importance of angiogenesis in tumour development has lead to the development of anti-angiogenic strategies to inhibit tumour growth. In this study, Polyphyllin D (PD), an active component in Chinese herb, Paris polyphylla, was evaluated for its potential anti-angiogenic effects.
METHODS AND RESULTS:
The inhibitory effects of Polyphyllin D on three important processes involved in angiogenesis, i.e. proliferation, migration and differentiation were examined using human microvascular endothelial cell line HMEC-1 by MTT assay, scratch assay and tube formation assay, respectively. Using zebrafish embryos as an animal model of angiogenesis, the anti-angiogenic effect of Polyphyllin D was further verified in vivo. Polyphyllin D suppressed the growth of HMEC-1 cells at 0.1-0.4 μM without toxic effects. At 0.3 μM and 0.4 μM, Polyphyllin D significantly inhibited endothelial cell migration and capillary tube formation. About 70% of the zebrafish embryos showed defects in intersegmental vessel formation upon treatment with Polyphyllin D at concentrations of 0.156 μM and 0.313 μM.
CONCLUSIONS:
The anti-angiogenic effects of Polyphyllin D have been explored in the study which implied a potential therapeutic development of Polyphyllin D in cancer treatment.
Biomed Pharmacother . 2019 Sep;117:109189.
Polyphyllin I induces autophagy and cell cycle arrest via inhibiting PDK1/Akt/mTOR signal and downregulating cyclin B1 in human gastric carcinoma HGC-27 cells[Pubmed: 31387191]
Abstract Paris polyphylla. is a traditional medicinal herb that has long been used to prevent cancer in many Asian countries. Polyphyllin I (PPI), an important bioactive constituent of Paris polyphylla, has been found to exhibit a wide variety of anticancer activities in many types of cancer cells. However, the effects of PPI on human gastric carcinoma cells and its mechanism of action remain unclear. In this study, we examined the effective anti-gastric carcinoma activity of PPI and its underlying mechanism of action in HGC-27 cells. In vitro, sub-micromolar concentrations of PPI inhibited HGC-27 cell proliferation with an IC50 of 0.34 ± 0.06 μM after a 72-h treatment. In vivo, 3 mg/kg PPI significantly inhibited proliferation of HGC-27 tumor cells, with a 78.8% inhibition rate compared to paclitaxel, and demonstrated higher safety. Analysis of MDC and mGFP-LC3 fluorescence, Western blotting and flow cytometry indicated that PPI induced cell cycle arrest in HGC-27 cells by promoting the conversion of LC3-I to LC3-II and by downregulating cyclin B1. Furthermore, Western blotting showed that PPI inhibited the autophagy-regulating PDK1/Akt/mTOR signaling pathway in vitro and in vivo. In addition, immunohistochemistry and TUNEL staining revealed that PPI decreased Ki67 expression and increased the percentage of apoptotic cells in HGC-27 xenograft tumors. These data indicate that PPI is an PDK1/Akt/mTOR signaling inhibitor and of therapeutic relevance for gastric cancer treatment and that the rhizome of Paris polyphylla deserves further clinical investigation as an alternative therapy for gastric cancer. Keywords: Autophagy; Cell cycle; Gastric cancer; PDK1/Akt/mTOR; Polyphyllin I.
Polyphyllin D Description
Source: The rhizomes of Paris yunnanensis Franch.
Solvent: DMSO, Pyridine, Methanol, Ethanol, 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).

Wherever 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: service@chemfaces.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.
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Calculate Dilution Ratios(Only for Reference)
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 need to make the dilution ratios of the samples. The dilution data of the sheet for your reference. Normally, it's can get a better solubility within lower of Concentrations.
Protocol
Kinase Assay:
J Med Food. 2014 Sep;17(9):1036-42.
Polyphyllin D induces apoptosis in U87 human glioma cells through the c-Jun NH2-terminal kinase pathway.[Pubmed: 25045920]
Polyphyllin D (PD), an active component from a traditional medicinal herb Paris polyphylla, which has long been used for the treatment of cancer in Asian countries, has been found to hold significant antitumor activity in vivo or in vitro. However, there were few reports on the effects and underlying mechanism of Polyphyllin D on apoptosis in U87 human glioma cells.
METHODS AND RESULTS:
The present study was conducted to evaluate apoptotic induction of Polyphyllin D in U87 human glioma cells, and explore its underlying pathway. U87 glioma cells were cultured and treated with varied concentrations of Polyphyllin D (from 10(-8) to 10(-4) M). The inhibition of U87 glioma cell proliferation by Polyphyllin D was assessed by MTT assay. The apoptosis of U87 glioma cells was detected by flow cytometry, and western blot analysis was used to examine human B-cell leukemia/lymphoma 2 (Bcl-2), human Bcl-2 associated X protein (Bax), caspase-3, total-c-jun NH2-terminal kinase (t-JNK), and phosphorylation-JNK (p-JNK) protein expression in U87 human glioma cells. The treatment with Polyphyllin D for 24 h significantly inhibited the proliferation of U87 human glioma cells in a concentration-dependent manner. Polyphyllin D increased apoptosis and significantly upregulated the expression of Bax, caspase-3, and p-JNK associated with apoptosis, but downregulated antiapoptotic Bcl-2 expression in U87 human glioma cells.
CONCLUSIONS:
Our data provided evidences that Polyphyllin D induces apoptosis in U87 human glioma cells. This effect might be associated with the JNK pathway.
Cell Research:
J Int Med Res. 2009 May-Jun;37(3):631-40.
Polyphyllin D exerts potent anti-tumour effects on Lewis cancer cells under hypoxic conditions.[Pubmed: 19589245]
Paris polyphylla has been used to treat cancer in China for many years and components of the plant, such as Polyphyllin D, may have potent antiproliferative effects in vitro.
METHODS AND RESULTS:
To investigate the potential antitumour effects of Polyphyllin D on cancer cells under hypoxia, Lewis lung cancer cells and mouse tracheal epithelial cells were cultured with or without Polyphyllin D under normoxic and hypoxic conditions. Proliferation and apoptosis of cells were assayed. Real-time reverse transcription-polymerase chain reaction was used to quantify the expression of hypoxia-inducible factor 1 alpha (HIF-1alpha) and vascular endothelial growth factor (VEGF) mRNA. Polyphyllin D decreased cell proliferation, increased apoptosis and inhibited expression of HIF-1alpha and VEGF mRNAs in Lewis cells. These effects were greater under hypoxic than normoxic conditions. Polyphyllin D did not show a cytotoxic effect in non-tumour cells (mouse skin fibroblasts and tracheal epithelial cells).
CONCLUSIONS:
These results suggest that Polyphyllin D potentially has anticancer effects in vitro under hypoxia.
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