Ponicidin

CAS# 52617-37-5

Ponicidin

Catalog No. BCN3231----Order now to get a substantial discount!

Product Name & Size Price Stock
Ponicidin: 5mg $173 In Stock
Ponicidin: 10mg Please Inquire In Stock
Ponicidin: 20mg Please Inquire Please Inquire
Ponicidin: 50mg Please Inquire Please Inquire
Ponicidin: 100mg Please Inquire Please Inquire
Ponicidin: 200mg Please Inquire Please Inquire
Ponicidin: 500mg Please Inquire Please Inquire
Ponicidin: 1000mg Please Inquire Please Inquire

Quality Control of Ponicidin

Number of papers citing our products

Chemical structure

Ponicidin

3D structure

Chemical Properties of Ponicidin

Cas No. 52617-37-5 SDF Download SDF
PubChem ID 92043456 Appearance Cryst.
Formula C20H26O6 M.Wt 362.4
Type of Compound Diterpenoids Storage Desiccate at -20°C
Synonyms Rubescensin B
Solubility Soluble in Chloroform,Dichloromethane,Ethyl Acetate,DMSO,Acetone,etc.
Chemical Name (1R,2S,8R,9S,11S,13S,14S,15R,19S)-13,14,19-trihydroxy-16,16-dimethyl-6-methylidene-10,12-dioxahexacyclo[9.8.0.01,15.02,8.05,9.08,13]nonadecan-7-one
SMILES CC1(CCC(C23C1C(C4(C56C2CCC(C5OC3O4)C(=C)C6=O)O)O)O)C
Standard InChIKey WHRDRHNMTIXZNY-CJZVHFPTSA-N
Standard InChI InChI=1S/C20H26O6/c1-8-9-4-5-10-18-11(21)6-7-17(2,3)12(18)14(23)20(24)19(10,13(8)22)15(9)25-16(18)26-20/h9-12,14-16,21,23-24H,1,4-7H2,2-3H3/t9?,10-,11-,12+,14-,15-,16-,18-,19-,20+/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.
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.

Source of Ponicidin

The herbs of Isodon japonicus

Biological Activity of Ponicidin

Description1. Ponicidin has immunoregulatory and anti-inflammatory functions . 2. Ponicidin has anti-viral function especially in the upper respiratory tract infection. 3. Ponicidin has anti-leukemia activity, by inducing apoptosis, downregulation of survivin as well as Bcl-2 expressions. 4. Ponicidin has anti-cancer activity against gastric carcinoma and lung cancer; can inhibit growth and induce apoptosis of gastric carcinoma cell line MKN28, via the signaling pathway regulated by Janus kinase 2 (JAK2) and signal transducers and activators of transcription 3 (STAT3).
TargetsROS | Bcl-2/Bax | Caspase | JAK | STAT | PI3K | Akt | ERK | JNK | HSV | PARP

Ponicidin Dilution Calculator

Concentration (start)
x
Volume (start)
=
Concentration (final)
x
Volume (final)
 
 
 
C1
V1
C2
V2

calculate

Ponicidin Molarity Calculator

Mass
=
Concentration
x
Volume
x
MW*
 
 
 
g/mol

calculate

Preparing Stock Solutions of Ponicidin

1 mg 5 mg 10 mg 20 mg 25 mg
1 mM 2.7594 mL 13.7969 mL 27.5938 mL 55.1876 mL 68.9845 mL
5 mM 0.5519 mL 2.7594 mL 5.5188 mL 11.0375 mL 13.7969 mL
10 mM 0.2759 mL 1.3797 mL 2.7594 mL 5.5188 mL 6.8985 mL
50 mM 0.0552 mL 0.2759 mL 0.5519 mL 1.1038 mL 1.3797 mL
100 mM 0.0276 mL 0.138 mL 0.2759 mL 0.5519 mL 0.6898 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.

Organizitions Citing Our Products recently

 
 
 

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
TsingHua University
The University of Michigan
The University of Michigan
Miami University
Miami University
DRURY University
DRURY University
Jilin University
Jilin University
Fudan University
Fudan University
Wuhan University
Wuhan University
Sun Yat-sen University
Sun Yat-sen University
Universite de Paris
Universite de Paris
Deemed University
Deemed University
Auckland University
Auckland University
The University of Tokyo
The University of Tokyo
Korea University
Korea University
Featured Products
New Products
 

References on Ponicidin

Ponicidin induces apoptosis via JAK2 and STAT3 signaling pathways in gastric carcinoma.[Pubmed:25588213]

Int J Mol Sci. 2015 Jan 12;16(1):1576-89.

Ponicidin has a variety of biological effects such as immunoregulatory and anti-inflammatory functions as well as anti-viral functions especially in the upper respiratory tract infection. This study was aimed to elucidate the antitumor effect of Ponicidin in gastric carcinoma MKN28 cells and the possible molecular mechanism involved. Cell viability was measured by the Cell Count Kit-8 (CCK8). Cell apoptosis was assessed by flow cytometry as well as cell cycle and reactive oxygen species (ROS) analysis. Western blot analysis was used to detect the active form of caspase-3 as well as Bax and B-cell lymphoma-2 (Bcl-2) expressions after cells were treated with different concentrations of Ponicidin. The results revealed that Ponicidin could inhibit the growth of MKN28 cells significantly in both a time- and dose-dependent manner. The cell cycle was blocked and ROS generation was increased after the cells were treated with Ponicidin. Bcl-2 expression was down-regulated remarkably while Bax expression and the active form of caspase-3 were increased after apoptosis occurred. We therefore conclude that Ponicidin exhibited significant growth inhibition of gastric carcinoma cell line MKN28 and induced apoptosis of MKN28 cells via the signaling pathway regulated by Janus kinase 2 (JAK2) and signal transducers and activators of transcription 3 (STAT3). Ponicidin may serve as a potential therapeutic agent for gastric carcinoma.

[Apoptosis inducing effect of ponicidin in leukemia K562 cells and its mechanisms of action].[Pubmed:21046753]

Zhongguo Zhong Yao Za Zhi. 2010 Aug;35(16):2161-5.

OBJECTIVE: To investigate the apoptosis inducing effects of Ponicidin (PON) on leukemic K562 cells and its mechanisms of action. METHOD: K562 cells in culture medium in vitro were given different concentrations of PON (10-50 micromol x L(-1)) for 24, 48 and 72 h. The inhibitory rate of the cells was measured by MTT assay, cell apoptotic rates were detected by flow cytometry (FCM) using Annexin V staining after K562 cells were treated with different concentrations of PON for 72 hours, and cell morphology was observed by Wright-Giemsa staining. Western blot was used to detect caspase-3 and poly(ADP-ribose) polymerase (PARP) expression, and the protein levels in mitogen-activated protein kinase signaling pathways (MAPKs, p-P38, p-ERK and p-JNK) as well as p-AKT and p-P85 in PI3K/AKT signaling pathways were also detected. RESULT: PON (over 30 micromol x L(-1)) could inhibit the growth of K562 cells in both time- and dose-dependent manner. FCM analysis revealed that apoptotic cells were gradually increased in a dose-dependent manner after treatment for 72 hours, and that marked morphological changes of cell apoptosis such as condensation of chromatin was clearly observed by Wright-Giemsa staining after treatment by 50 micromol x L(-1) PON. Western blot showed cleavage of the caspase-3 zymogen protein (32 kD), with the appearance of its 17 kD subunit, and a cleaved 89 kD fragment of 116 kD PARP was also found. Furthermore, Western blotting also showed that expression of p-AKT and p-P85 in PI3K/AKT signaling pathways was downregulated dramatically whereas the expression of p-P38 as well as p-ERK and p-JNK remained unchanged after the cells were treated by PON for 48 h. CONCLUSION: The results demonstrate that PON exhibits in vitro anti-leukemia effect by induction of apoptosis in K562 cells, and that PON induced apoptosis in K562 cells mainly related to activation of caspase-3 as well as inactivation of PI3K/AKT signaling pathway via down regulation of the expression of p-AKT and p-P85 protein levels. These results provide strong laboratory evidence for further anti-leukemia trials of PON.

Ponicidin, an ent-kaurane diterpenoid derived from a constituent of the herbal supplement PC-SPES, Rabdosia rubescens, induces apoptosis by activation of caspase-3 and mitochondrial events in lung cancer cells in vitro.[Pubmed:16537182]

Cancer Invest. 2006 Mar;24(2):136-48.

Ponicidin, an ent-kaurane diterpenoid derived from a constituent of the herbal supplement PC-SPES, Rabdosia rubescens, is recently reported to have anti-tumor effects on a large variety of cancers. In this study, we demonstrate that Ponicidin exhibits cytotoxicity, induces apoptosis, disrupts the mitochondrial membrane potential, and triggers the activation of caspase-3, -8 and -9 in lung cancer A549 and GLC-82 cells. Ponicidin treatment of lung cancer cells caused downregulation of anti-apoptotic protein Bcl-2 and survivin as well as upregulaton of pro-apoptotic protein Bax in a time dependent manner when apoptosis ocurred. Ponicidin induced activation of caspase-3 can be blocked by a caspase-3-specific inhibitor z-DEVD-FMK Furthermore, the caspase-8-specific inhibitor z-IETD-FMK could block the Ponicidin-induced activation of caspase-3, PARP cleavage, and prevented the release of cytochrome c from mitochondria into the cytoplasm. This indicate that activated caspase-8 initiates the release of cytochrome c during Ponicidin-induced apoptosis. We therefore conclude that Ponicidin has significant apoptosis-inducing effects by activation of caspase-3 -8, and -9 as well as downregulation of anti-apoptotic protein Bcl-2, survivin and upregulation of pro-apoptotic protein Bax, with caspase-8 acting as an upstream activator. The data offer a potential mechanism for Ponicidin-induced apoptosis in lung cancer cells, suggesting that Ponicidin may severve as an effective reagent for the treatment of lung cancer, and that in vivo anti-cancer effects as well as its potential clinical effectiveness need further investigation.

Potentiation of ganciclovir toxicity in the herpes simplex virus thymidine kinase/ganciclovir administration system by ponicidin.[Pubmed:10678355]

Cancer Gene Ther. 2000 Jan;7(1):45-52.

The herpes simplex virus thymidine kinase (HSV-TK)/ganciclovir (GCV) administration system is commonly used in gene therapy trials. We have evaluated the effect of Ponicidin, a diterpenoid isolated from a plant, Rabdosia ternifolia, on the cell-killing activity of the anti-herpes drugs acyclovir (ACV) and GCV. Ponicidin preferentially activated HSV-1-specific TK but not cellular kinases. In HSV-infected cells, Ponicidin significantly accumulated the phosphorylated metabolites of GCV and suppressed the extracellular release of GCV. These data suggested that the cytotoxicities of ACV and GCV in HSV-TK-expressing cells might be potentiated by Ponicidin. After transfected with the HSV-1 TK gene, COS-1 and several human cancer cells became highly sensitive to the cytotoxic properties of the nucleoside analogs. When Ponicidin at the concentration without antiviral activities (0.2 microg/mL) was combined with ACV or GCV, the cytotoxic levels in HSV-TK-expressing cells were enhanced by 3- to 87-fold and 5- to 52-fold, respectively, compared with the nucleoside alone. When the stability of the bioactivity of Ponicidin in the blood of mice was evaluated, the substance showed relatively long-lasting effects on the potentiation of the anti-herpetic and cytotoxic activities of GCV after intravenous administration. These data suggest that the combined use of Ponicidin with GCV will be effective for cancer gene therapy, because high cytotoxicity in viral TK-expressing cells should yield more rapid and enhanced tumor elimination.

Ponicidin inhibits monocytic leukemia cell growth by induction of apoptosis.[Pubmed:19330074]

Int J Mol Sci. 2008 Nov;9(11):2265-77.

In this study two monocytic leukemia cell lines, U937 and THP-1 cells, were used to investigate the anti-proliferation effects caused by Ponicidin. Cell viability was measured by an MTT assay. Cell apoptosis was assessed by flow cytometry as well as DNA fragmentation analysis. Cell morphology was observed using an inverted microscope and Hoechst 33258 staining. RT-PCR and Western blot analysis were used to detect survivin as well as Bax and Bcl-2 expressions after the cells were treated with different concentrations of Ponicidin. The results revealed that Ponicidin could inhibit the growth of U937 and THP-1 cells significantly by induction of apoptosis. The suppression was in both time- and dose-dependent manner. Marked morphological changes of cell apoptosis were observed clearly after the cells were treated with Ponicidin for 48 approximately 72 h. RT-PCR and Western blot analysis demonstrated that both survivin and Bcl-2 expressions were down-regulated remarkably while Bax expression remained constant before and after apoptosis occurred. We therefore conclude that Ponicidin has significant anti-proliferation effects by inducing apoptosis on leukemia cells in vitro, downregulation of survivin as well as Bcl-2 expressions may be the important apoptosis inducing mechanisms. The results suggest that Ponicidin may serve as potential therapeutic agent for leukemia.

Description

Ponicidin (Rubescensine B) is a diterpenoid derived from Rabdosia rubescens, and exhibits immunoregulatory, anti-inflammatory, anti-viral and anti-cancer activity. Ponicidin (Rubescensine B) induces apoptosis of gastric carcinoma cell, decreases the phosphorylation of JAK2 and STAT3, and shows no effect on protein levels of JAK2 and STAT3.

Keywords:

Ponicidin,52617-37-5,Rubescensin B,Natural Products, buy Ponicidin , Ponicidin supplier , purchase Ponicidin , Ponicidin cost , Ponicidin manufacturer , order Ponicidin , high purity Ponicidin

Online Inquiry for:

      Fill out the information below

      • Size:Qty: - +

      * Required Fields

                                      Result: