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Periplocin
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Product Name Periplocin
Price: $80 / 20mg
CAS No.: 13137-64-9
Catalog No.: CFN90513
Molecular Formula: C36H56O13
Molecular Weight: 696.82 g/mol
Purity: >=98%
Type of Compound: Steroids
Physical Desc.: Powder
Source: The root barks of Periploca sepium Bunge.
Solvent: DMSO, Pyridine, Methanol, Ethanol, etc.
Download: COA    MSDS    SDF
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: Periplocin has anti-cancer, and potent immunoregulatory effects, it induces apoptosis and inhibits growth of cancer cells by the beta-catenin/Tcf signaling pathway. Periplocin is used for treatment of rheumatoid arthritis, reinforcement of bones and tendons, palpitations or shortness of breath and lower extremity edema in traditional medicine.
Targets: Akt | ERK | Bcl-2/Bax | Caspase | Wnt/β-catenin | TNF-α | IL Receptor
In vitro:
Cell Physiol Biochem. 2014;33(3):859-68.
Comparative proteomic analysis of anti-cancer mechanism by periplocin treatment in lung cancer cells.[Pubmed: 24685647]
Periplocin is used for treatment of rheumatoid arthritis, reinforcement of bones and tendons, palpitations or shortness of breath and lower extremity edema in traditional medicine. Our previous findings suggested that Periplocin could inhibit the growth of lung cancer both in vitro and in vivo. But the biological processes and molecular pathways by which Periplocin induces these beneficial effects remain largely undefined.
METHODS AND RESULTS:
To explore the molecular mechanisms of Periplocin involved in anti-cancer activity, in the present study the protein profile changes of human lung cancer cell lines A549 in response to Periplocin treatment were investigated using the proteomics approaches (2-DE combined with MS/MS). Western blot was employed to verify the changed proteins. Interactions between changed proteins were analyzed by STRING. 29 down-regulated protein species named GTP-binding nuclear protein Ran (RAN), Rho GDP-dissociation inhibitor 1 (ARHGDIA), eukaryotic translation initiation factor 5A-1 (EIF5A) and Profilin-1(PFN1), and 10 up-regulated protein species named Heat shock cognate 71 kDa protein (HSPA8),10 kDa heat shock protein (HSPE1), and Cofilin-1(CFL-1) were identified. Among them, GTP-binding nuclear protein Ran (RAN) and Rho GDP-dissociation inhibitor 1 (ARHGDIA) were the most significantly changed (over tenfold). The proteasome subunit beta type-6 (PSMB6), ATP synthase ecto-α-subunit (ATP5A1), Aldehyde dehydrogenase 1 (ALDH1) and EIF5A were verified by immunoblot assays to be dramatically down-regulated. By STRING bioinformatics analysis revealing interactions and signaling networks it became apparent that the proteins changed they are primarily involved in transcription and proteolysis.
CONCLUSIONS:
Periplocin inhibited growth of lung cancer by down-regulating proteins, such as ATP5A1, EIF5A, ALDH1 and PSMB6. These findings may improve our understanding of the molecular mechanisms underlying the anti-cancer effects of Periplocin on lung cancer cells.
In vivo:
Evid Based Complement Alternat Med. 2013;2013:958025.
Antitumor Effect of Periplocin in TRAIL-Resistant Human Hepatocellular Carcinoma Cells through Downregulation of IAPs.[Pubmed: 23365613]
Cortex periplocae is the dried root bark of Periploca sepium Bge., a traditional Chinese herb medicine. It contains high amounts of cardiac glycosides. Several cardiac glycosides have been reported to inhibit tumor growth or induce tumor cell apoptosis.
METHODS AND RESULTS:
We extracted and purified cortex periplocae and identified Periplocin as the active ingredient that inhibited the growth of TNF-related apoptosis-inducing ligand-(TRAIL-) resistant hepatocellular carcinoma cells. The antitumor activity of Periplocin was further increased by TRAIL cotreatment. Periplocin sensitized TRAIL-resistant HCC through the following two mechanisms. First, Periplocin induced the expression of DR4 and FADD. Second, the cotreatment of TRAIL and Periplocin suppressed several inhibitors of apoptosis (IAPs). Both mechanisms resulted in the activation of caspase 3, 8, and 9 and led to cell apoptosis. In addition, intraperitoneal injection (IP) of Periplocin repressed the growth of hepatocellular carcinoma (HCC) in xenograft tumor model in mice.
CONCLUSIONS:
In summary, Periplocin sensitized TRAIL-resistant HCC cells to TRAIL treatment and resulted in tumor cell apoptosis and the repression of tumor growth in vivo.
Periplocin Description
Source: The root barks of Periploca sepium Bunge.
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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Recently, ChemFaces products have been cited in many studies from excellent and top scientific journals

Cell. 2018 Jan 11;172(1-2):249-261.e12.
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Calculate Dilution Ratios(Only for Reference)
1 mg 5 mg 10 mg 20 mg 25 mg
1 mM 1.4351 mL 7.1755 mL 14.3509 mL 28.7018 mL 35.8773 mL
5 mM 0.287 mL 1.4351 mL 2.8702 mL 5.7404 mL 7.1755 mL
10 mM 0.1435 mL 0.7175 mL 1.4351 mL 2.8702 mL 3.5877 mL
50 mM 0.0287 mL 0.1435 mL 0.287 mL 0.574 mL 0.7175 mL
100 mM 0.0144 mL 0.0718 mL 0.1435 mL 0.287 mL 0.3588 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
Cell Research:
Oncol Rep. 2010 Aug;24(2):375-83.
Periplocin from Cortex periplocae inhibits cell growth and down-regulates survivin and c-myc expression in colon cancer in vitro and in vivo via beta-catenin/TCF signaling.[Pubmed: 20596624]
Cancer of the colon and rectum is the third most commonly diagnosed cancer and accounts for approximately 10% of all cancer-related deaths. Although surgical resection or radiotherapy are potentially curative for localized disease, advanced colon cancer is currently associated with poor prognosis. Therefore, the development of a new and effective chemotherapeutic agent is required to target critical pathways to induce responsiveness of colon cancer cells to death signals. Dysregulation of the beta-catenin/TCF pathway plays a central role in early activities of colorectal carcinogenesis.
METHODS AND RESULTS:
In this study, human colon cancer SW480 cells were used to investigate the effect of CPP (Periplocin from Cortex periplocae) on the modulation of the beta-catenin/TCF signaling pathway. Our research results showed that CPP caused a dose- and time-dependent inhibition of cell growth as assessed by MTT assay and an induction in apoptosis as measured by flow cytometry and transmission electron microscopy. Furthermore, the CPP- treated cells were characterized by a decreased expression of beta-catenin protein in the total cell lysates and cytosolic and nuclear extracts. This expression alleviates the binding activity of T-cell factor (Tcf) complexes to its specific DNA-binding sites. Thus, the protein expression of the downstream elements survivin and c-myc was down-regulated. To determine the precise inhibitory mechanisms involved, further in-depth in vivo studies of CPP are warranted.
METHODS AND RESULTS:
In conclusion, our data suggest that CPP wields a multi-prong strategy to target the beta-catenin/Tcf signaling pathway, leading to the induction of apoptosis and inhibition of growth of colon cancer cells in vitro and in vivo. Therefore, CPP may become a potential agent against colon cancer.
Animal Research:
Xi Bao Yu Fen Zi Mian Yi Xue Za Zhi. 2009 Oct;25(10):887-90.
Immunoregulatory effects of periplocin from Cortex Periplocae in tumor-bearing mice.[Pubmed: 19811733]
To investigate the immune mechanisms for Periplocin from Cortex Periplocae (CPP) in tumor-bearing mice.
METHODS AND RESULTS:
H(22) tumor-bearing model BALB/c mice were applied to evaluated in vivo immunoregulatory effect of CPP. The influence of different dose CPP (0.25, 0.50 and 1.00 mg/kg) on immune organs in tumor-bearing mice were observed. T cell subsets of mice spleen were detected by flow cytometry. MTT assay was used to determine the influence of CPP on lymphocyte proliferation of mice spleen stimulated by ConA. The levels of TNF-alpha, IL-2 and IL-12 in serum from mice were detected by means of ELISA. Thymus index and spleen index of H(22) tumor-bearing model control mice became less than that of normal mice (P<0.05). Compared to both model and normal control groups, thymus index and spleen index of H(22) tumor-bearing mice treated with CPP increased obviously (P<0.05). CPP had no influence on the number of CD8(+) T cells, but up-regulated markedly the number of CD3(+), CD4(+) T cells and the ratio of CD4(+)/CD8(+) in tumor-bearing mice. In CPP-treated mice, the percentage of CD3(+), CD4(+) T cells were not different from normal mice (P<0.05), the ratio of CD4(+)/CD8(+) was higher than that of normal mice (P<0.05). CPP enhanced obviously lymphocyte proliferation of mice spleen induced by ConA, the SI scores were even higher than that of normal mice. The levels of TNF-alpha, IL-2 and IL-12 in serum from CPP-treated mice, increased significantly compared to model control group (P<0.05) in a dose-dependent manner, were similar to or higher than that of normal mice.
CONCLUSIONS:
CPP protected immune organs of tumor-bearing mice, increased obviously the percentage of CD4(+) and CD4(+)/CD8(+) among the T cell line, and enhanced lymphocyte proliferation of mice spleen significantly, stimulated the production of TNF-alpha, IL-2 and IL-12. The results suggested that CPP possessed potent immunoregulatory effect.
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