番泻苷B
Sennoside B
|
产品编号 |
CFN99904 |
CAS编号 |
128-57-4 |
分子式 = 分子量 |
C42H38O20 = 862.74 |
产品纯度 |
>=98% |
物理属性 |
Yellow powder |
化合物类型 |
Anthraquinones |
植物来源 |
The leaves of Cassia angustifolia. |
ChemFaces的产品在影响因子大于5的优秀和顶级科学期刊中被引用 |
|
产品名称 |
产品编号 |
CAS编号 |
包装 |
QQ客服 |
番泻苷B |
CFN99904 |
128-57-4 |
10mg |
QQ客服:215959384 |
番泻苷B |
CFN99904 |
128-57-4 |
20mg |
QQ客服:215959384 |
番泻苷B |
CFN99904 |
128-57-4 |
50mg |
QQ客服:215959384 |
番泻苷B |
CFN99904 |
128-57-4 |
100mg |
QQ客服:215959384 |
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ChemFaces的产品在许多优秀和顶级科学期刊中被引用
Cell. 2018 Jan 11;172(1-2):249-261.e12. doi: 10.1016/j.cell.2017.12.019.
IF=36.216(2019)PMID: 29328914
Cell Metab. 2020 Mar 3;31(3):534-548.e5. doi: 10.1016/j.cmet.2020.01.002.
IF=22.415(2019)PMID: 32004475
Mol Cell. 2017 Nov 16;68(4):673-685.e6. doi: 10.1016/j.molcel.2017.10.022.
IF=14.548(2019)PMID: 29149595
ACS Nano. 2018 Apr 24;12(4): 3385-3396. doi: 10.1021/acsnano.7b08969.
IF=13.903(2019)PMID: 29553709
Nature Plants. 2016 Dec 22;3: 16206. doi: 10.1038/nplants.2016.205.
IF=13.297(2019)PMID: 28005066
Sci Adv. 2018 Oct 24;4(10): eaat6994. doi: 10.1126/sciadv.aat6994.
IF=12.804(2019)PMID: 30417089
我们的产品现已经出口到下面的研究机构与大学,并且还在增涨
Korea Intitute of Science and Technology (KIST) (Korea)
Funda??o Universitária de Desenvolvimento (Brazil)
Uniwersytet Medyczny w ?odzi (Poland)
Osmania University (India)
Univerzita Karlova v Praze (Czech Republic)
Florida International University (USA)
Shanghai Institute of Organic Chemistry (China)
Copenhagen University (Denmark)
Massachusetts General Hospital (USA)
Shanghai University of TCM (China)
Sant Gadge Baba Amravati University (India)
Georgia Institute of Technology (USA)
University of Cincinnati (USA)
University of Malaya (Malaysia)
More...
国外学术期刊发表的引用ChemFaces产品的部分文献
Description: |
Sennoside B, a major purgative component, has a potential utility in the treatment of proliferative diseases, through inhibiting PDGF-stimulated cell proliferation by binding to PDGF-BB and its receptor and by down-regulating the PDGFR-beta signaling pathway. It and sennoside A also possess significant gastroprotective activities . |
Targets: |
PGE | ATPase | Potassium Channel | PDGFR | STAT | ERK | Akt |
In vitro: |
Life Sci. 2009 Jun 19;84(25-26):915-22. | Sennoside B inhibits PDGF receptor signaling and cell proliferation induced by PDGF-BB in human osteosarcoma cells.[Pubmed: 19393247] | AIMS:
To address the possibility that sennoside B inhibition of cell proliferation is mediated via interference with platelet-derived growth factor (PDGF) signaling.
MAIN METHODS:
Human osteosarcoma MG63 cells were treated with PDGF in the presence or absence of sennoside B. Activation of the PDGF signaling pathway was monitored using western immunoblotting with specific antibodies against the PDGF receptor, phosphotyrosine and components of the downstream signaling cascade. Activation of cell metabolism and proliferation was assessed by chromogenic reduction of MTT.
KEY FINDINGS:
Sennoside B was found to inhibit PDGF-BB-induced phosphorylation of the PDGF receptor (PDGFR) in human MG63 osteosarcoma cells. Downstream signaling was also affected; pre-incubation of PDGF-BB with sennoside B inhibited the phosphorylation of pathway components including Ak strain To address the possibility that Sennoside B inhibition of cell proliferation is mediated via interference with platelet-derived growth factor (PDGF) signaling.
METHODS AND RESULTS: Human osteosarcoma MG63 cells were treated with PDGF in the presence or absence of Sennoside B. Activation of the PDGF signaling pathway was monitored using western immunoblotting with specific antibodies against the PDGF receptor, phosphotyrosine and components of the downstream signaling cascade. Activation of cell metabolism and proliferation was assessed by chromogenic reduction of MTT. Sennoside B was found to inhibit PDGF-BB-induced phosphorylation of the PDGF receptor (PDGFR) in human MG63 osteosarcoma cells. Downstream signaling was also affected; pre-incubation of PDGF-BB with Sennoside B inhibited the phosphorylation of pathway components including Ak strain transforming protein (AKT), signal transducer and activator of transcription 5 (STAT-5) and extracellular signal-regulated kinase 1/2 (ERK1/2). Further, we found that Sennoside B can bind directly to the extracellular domains of both PDGF-BB and the PDGF-beta receptor (PDGFR-beta). The effect was specific for Sennoside B; other similar compounds including aloe-emodin, rhein and the meso isomer (sennoside A) failed to inhibit PDGFR activation or downstream signaling. Sennoside B also inhibited PDGF-BB stimulation of MG63 cell proliferation. CONCLUSIONS: These results indicate that Sennoside B can inhibit PDGF-stimulated cell proliferation by binding to PDGF-BB and its receptor and by down-regulating the PDGFR-beta signaling pathway. Sennoside B is therefore of potential utility in the treatment of proliferative diseases in which PDGF signaling plays a central role. |
|
In vivo: |
J Drug Target. 2015 Feb;23(2):180-90. | Experimental evaluation of radioiodinated sennoside B as a necrosis-avid tracer agent.[Pubmed: 25330022] | Necrosis-avid agents are a class of compounds that selectively accumulate in the necrotic tissues after systemic administration, which can be used for in vivo necrosis imaging and targeted therapies.
METHODS AND RESULTS:
In order to search for a necrosis-avid tracer agent with improved drugability, we labelled iodine-131 on Sennoside B (SB) as a naturally occurring median dianthrone compound. The necrosis targetability and clearance properties of (131)I-Sennoside B were evaluated in model rats with liver and muscle necrosis. On SPECT/CT images, a "hot spot" in the infarcted liver lobe and necrotic muscle was persistently observed at 24 h and 72 h post-injection (p.i.). Gamma counting of the tissues of interest revealed a radioactivity ratio of necrotic to viable liver at 4.6 and 3.4 and of necrotic to viable muscle at 7.0 and 8.8 at 24 h and 72 h p.i., respectively. The good match of autoradiographs and fluoromicroscopic images with corresponding histochemical staining suggested preferential uptake of (131)I-Sennoside B in necrotic tissue. Pharmacokinetic study revealed that (131)I-Sennoside B has an elimination half-life of 8.6 h.
CONCLUSIONS:
This study indicates that (131)I-Sennoside B shows not only prominent necrosis avidity but also favourable pharmacokinetics, which may serve as a potential necrosis-avid diagnostic agent for assessment of tissue viability. |
|
|
1 mg |
5 mg |
10 mg |
20 mg |
25 mg |
1 mM |
1.1591 mL |
5.7955 mL |
11.591 mL |
23.182 mL |
28.9774 mL |
5 mM |
0.2318 mL |
1.1591 mL |
2.3182 mL |
4.6364 mL |
5.7955 mL |
10 mM |
0.1159 mL |
0.5795 mL |
1.1591 mL |
2.3182 mL |
2.8977 mL |
50 mM |
0.0232 mL |
0.1159 mL |
0.2318 mL |
0.4636 mL |
0.5795 mL |
100 mM |
0.0116 mL |
0.058 mL |
0.1159 mL |
0.2318 mL |
0.2898 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.
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