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Eriocalyxin B
Eriocalyxin B
ChemFaces products have been cited in many studies from excellent and top scientific journals
Product Name Eriocalyxin B
Price:
CAS No.: 84745-95-9
Catalog No.: CFN97402
Molecular Formula: C20H24O5
Molecular Weight: 344.4 g/mol
Purity: >=98%
Type of Compound: Diterpenoids
Physical Desc.: Powder
Source: The herbs of Isodon eriocalyx.
Solvent: Chloroform, Dichloromethane, Ethyl Acetate, DMSO, Acetone, etc.
Download: COA    MSDS    SDF    Manual
Similar structural: Comparison (Web)  (SDF)
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Related Screening Libraries
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10 mM * 1 mL in DMSO / Inquiry / In-stock
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Biological Activity
Description: Eriocalyxin B induces apoptosis and cell cycle arrest in pancreatic adenocarcinoma cells through caspase- and p53-dependent pathways, should be considered a candidate for pancreatic cancer treatment; it is a specific inhibitor of STAT3, it directly targets STAT3 through a covalent linkage to inhibit the phosphorylation and activation of STAT3 and induces apoptosis of STAT3-dependent tumor cells. Eriocalyxin B exerts potent antiinflammatory effects through selective modulation of pathogenic Th1 and Th17 cells by targeting critical signaling pathways. Eriocalyxin B reversibly interfer with the binding of p65 and p50 subunits to the DNA in a noncompetitive manner.
Targets: STAT | cAMP | p65 | Bcl-2/Bax | Caspase | p53 | NF-kB | TNF-α | COX | NOS | Akt | ERK
In vitro:
Proc Natl Acad Sci U S A. 2013 Feb 5;110(6):2258-63.
Eriocalyxin B ameliorates experimental autoimmune encephalomyelitis by suppressing Th1 and Th17 cells.[Pubmed: 23345445]
Eriocalyxin B (EriB), a diterpenoid isolated from Isodon eriocalyx, was previously reported to have antitumor effects via multiple pathways, and these pathways are related to immune responses.
METHODS AND RESULTS:
In this study, we demonstrated that Eriocalyxin B was efficacious in experimental autoimmune encephalomyelitis (EAE), an animal model for multiple sclerosis. Treatment with Eriocalyxin B led to amelioration of EAE, which correlated with reduced spinal cord inflammation and demyelination. Eriocalyxin B treatment abolished encephalitogenic T-cell responses to myelin oligodendrocyte glycoprotein in an adoptive transfer EAE model. The underlying mechanism of Eriocalyxin B-induced effects involved inhibition of T helper (Th) 1 and Th17 cell differentiation through Janus Kinase/Signal Transducer and Activator Of Transcription and Nuclear factor-κB signaling pathways as well as elevation of reactive oxygen species.
CONCLUSIONS:
These findings indicate that Eriocalyxin B exerts potent antiinflammatory effects through selective modulation of pathogenic Th1 and Th17 cells by targeting critical signaling pathways. The study provides insights into the role of Eriocalyxin B as a unique therapeutic agent for the treatment of autoimmune diseases.
Exp Hematol. 2010 Mar;38(3):191-201.
Eriocalyxin B induces apoptosis in lymphoma cells through multiple cellular signaling pathways.[Pubmed: 20045442]
Eriocalyxin B (EriB) is a natural diterpenoid purified from Isodon eriocalyx var. laxiflora and possesses strong antileukemic activity. In this study, we further investigated its effect and mechanism of action in human lymphoma.
METHODS AND RESULTS:
In vitro, a series of B- and T-lymphoma cells were treated with Eriocalyxin B. Eriocalyxin B significantly inhibited lymphoma cell proliferation and induced apoptosis in association with caspase activation. Meanwhile, multiple signal transduction pathways were involved in lymphoma cell apoptosis in response to Eriocalyxin B, including inhibition of nuclear factor (NF)-kappaB and AKT pathways, and the activation of extracellular signal-related kinase (ERK) pathway. ERK activation corresponded to reactive oxygen species production and could be blocked by antioxidant dithiothreitol. In murine xenograft lymphoma models, Eriocalyxin B remarkably inhibited tumor growth and induced in situ tumor cell apoptosis.
CONCLUSIONS:
These findings broaden the value of Eriocalyxin B as a promising candidate targeting apoptosis cascade in treatment of hematological malignancies.
Mol Pharmacol. 2006 Dec;70(6):1946-55.
Eriocalyxin B inhibits nuclear factor-kappaB activation by interfering with the binding of both p65 and p50 to the response element in a noncompetitive manner.[Pubmed: 16940413 ]
Nuclear factor-kappaB (NF-kappaB) has been recognized to play a critical role in cell survival and inflammatory processes. It has become a target for intense drug development for the treatment of cancer, inflammatory, and autoimmune diseases.
METHODS AND RESULTS:
Here, we describe a potent NF-kappaB inhibitor, Eriocalyxin B (Eri-B), an ent-kauranoid isolated from Isodon eriocalyx, an anti-inflammatory remedy. The presence of two alpha,beta-unsaturated ketones give this compound the uniqueness among the ent-kauranoids tested. Eri-B inhibited the NF-kappaB transcriptional activity but not that of cAMP response element-binding protein. It suppressed the transcription of NF-kappaB downstream gene products including cyclooxygenase-2 and inducible nitric-oxide synthase induced by tumor necrosis factor-alpha or lipopolysaccharide in macrophages and hepatocarcinoma cells. Chromatin immunoprecipitation assay indicated that Eri-B selectively blocked the binding between NF-kappaB and the response elements in vivo without affecting the nuclear translocation of the transcription factor. Down-regulation of the endogenous p65 protein sensitized the cells toward the action of the compound. Furthermore, in vitro binding assays suggested that Eri-B reversibly interfered with the binding of p65 and p50 subunits to the DNA in a noncompetitive manner.
CONCLUSIONS:
In summary, this study reveals the novel action of a potent NF-kappaB inhibitor that could be potentially used for the treatment of a variety of NF-kappaB-associated diseases. Modification of the structure of this class of compounds becomes the key to the control of the behavior of the compound against different cellular signaling pathways.
Nat Prod Bioprospect . 2020 Jun;10(3):131-140.
Eriocalyxin B Inhibits Adipogenesis in 3T3-L1 Adipocytes by Cell Cycle Arrest[Pubmed: 32314168]
Abstract Eriocalyxin B, an ent-Kaurene diterpenoid extracted from a traditional Chinese herb Isodon eriocalyx, has been shown to possess multifunctional activities such as anti-cancer and anti-inflammatory. However, the function and mechanism of the compound in adipocyte differentiation is still unknown. Here we reported that Eriocalyxin B blunted adipogenesis remarkably by inhibiting the accumulation of lipid droplets, triglycerides and the expressions of adipogenesis-related factors, including C/EBPβ, C/EBPα, PPARγ, and FABP4. Moreover, we showed that the inhibition might be the consequence of cell cycle being arrested at the G2/M phase during the mitotic clonal expansion of adipocyte differentiation, most likely by suppressing mRNAs and proteins of CDK1, CDK2, Cyclin A and Cyclin B1. Overall, we conclude that Eriocalyxin B is capable of inhibiting adipocyte differentiation at the early stage through downregulating the proteins involved in cell cycle progression. Keywords: Adipocyte differentiation; Cell cycle; Eriocalyxin B.
Eriocalyxin B Description
Source: The herbs of Isodon eriocalyx.
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).

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 2.9036 mL 14.518 mL 29.036 mL 58.072 mL 72.59 mL
5 mM 0.5807 mL 2.9036 mL 5.8072 mL 11.6144 mL 14.518 mL
10 mM 0.2904 mL 1.4518 mL 2.9036 mL 5.8072 mL 7.259 mL
50 mM 0.0581 mL 0.2904 mL 0.5807 mL 1.1614 mL 1.4518 mL
100 mM 0.029 mL 0.1452 mL 0.2904 mL 0.5807 mL 0.7259 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:
PLoS One. 2015 May 26;10(5):e0128406.
Eriocalyxin B Inhibits STAT3 Signaling by Covalently Targeting STAT3 and Blocking Phosphorylation and Activation of STAT3.[Pubmed: 26010889]
Activated STAT3 plays an important role in oncogenesis by stimulating cell proliferation and resisting apoptosis. STAT3 therefore is an attractive target for cancer therapy.
METHODS AND RESULTS:
We have screened a traditional Chinese herb medicine compound library and found Eriocalyxin B (EB), a diterpenoid from Isodon eriocalyx, as a specific inhibitor of STAT3. EB selectively inhibited constitutive as well as IL-6-induced phosphorylation of STAT3 and induced apoptosis of STAT3-dependent tumor cells. EB did not affect the upstream protein tyrosine kinases or the phosphatase (PTPase) of STAT3, but rather interacted directly with STAT3. The effects of EB could be abolished by DTT or GSH, suggesting a thiol-mediated covalent linkage between EB and STAT3. Site mutagenesis of cysteine in and near the SH2 domain of STAT3 identified Cys712 to be the critical amino acid for the EB-induced inactivation of STAT3. Furthermore, LC/MS/MS analyses demonstrated that an α, β-unsaturated carbonyl of EB covalently interacted with the Cys712 of STAT3. Computational modeling analyses also supported a direct interaction between EB and the Cys712 of STAT3.
CONCLUSIONS:
These data strongly suggest that EB directly targets STAT3 through a covalent linkage to inhibit the phosphorylation and activation of STAT3 and induces apoptosis of STAT3-dependent tumor cells.
Curr Mol Med. 2014;14(5):673-89.
Eriocalyxin B-induced apoptosis in pancreatic adenocarcinoma cells through thiol-containing antioxidant systems and downstream signalling pathways.[Pubmed: 24894173]
Our earlier studies have shown that Eriocalyxin B (EriB), a diterpenoid isolated from Isodon eriocalyx, possesses anti-pancreatic tumour activities in vitro and in vivo.
METHODS AND RESULTS:
The present study further demonstrated that only thiol-containing antioxidants, N-acetylcysteine (NAC) or dithiothreitol (DTT), inhibited EriB-induced cytotoxicity and apoptosis. Eriocalyxin B suppressed the glutathione and thioredoxin antioxidant systems, thus increasing the intracellular ROS levels and regulating the MAPK, NFκB pathways. In vivo studies also showed that Eriocalyxin B treatment (2.5 mg/kg) reduced the pancreatic tumour weights significantly in nude mice with increased superoxide levels.
CONCLUSIONS:
Taken together, our results shed important new light on the molecular mechanisms of Eriocalyxin B acting as an apoptogenic agent and its therapeutic potential for pancreatic cancer.
Toxicol Appl Pharmacol. 2012 Jul 1;262(1):80-90.
Eriocalyxin B induces apoptosis and cell cycle arrest in pancreatic adenocarcinoma cells through caspase- and p53-dependent pathways.[Pubmed: 22561874]
Eriocalyxin B (EriB), isolated from the Isodon eriocalyx plant, is an ent-kaurane diterpenoid with promise as a broad-spectrum anti-cancer agent. The anti-leukemic activity of Eriocalyxin B, including the underlying mechanisms involved, has been particularly well documented.
METHODS AND RESULTS:
In this study, we demonstrated for the first time Eriocalyxin B's potent cytotoxicity against four pancreatic adenocarcinoma cell lines, namely PANC-1, SW1990, CAPAN-1, and CAPAN-2. The effects were comparable to that of the chemotherapeutic camptothecin (CAM), but with much lower toxicity against normal human liver WRL68 cells. Eriocalyxin B's cytoxicity against CAPAN-2 cells was found to involve caspase-dependent apoptosis and cell cycle arrest at the G2/M phase. Moreover, the p53 pathway was found to be activated by Eriocalyxin B in these cells. Furthermore, in vivo studies showed that Eriocalyxin B inhibited the growth of human pancreatic tumor xenografts in BALB/c nude mice without significant secondary adverse effects.
CONCLUSIONS:
These results suggest that Eriocalyxin B should be considered a candidate for pancreatic cancer treatment.
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