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- 保存条件:
Powder: -20°C, 3 years; 4°C, 2 years.In solvent: -80°C, 6 months; -20°C, 1 month.
- 英文名:
Chrysophanic acid
- 库存:
货期:1-2天
- 供应商:
MedChemExpress LLC
- CAS号:
481-74-3
- 规格:
50 mg/100 mg/500 mg/1 g
| 规格: | 50 mg | 产品价格: | ¥400.0 |
|---|---|---|---|
| 规格: | 100 mg | 产品价格: | ¥600.0 |
| 规格: | 500 mg | 产品价格: | ¥2100.0 |
| 规格: | 1 g | 产品价格: | ¥3350.0 |
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Chrysophanol
CAS No. : 481-74-3
MCE 国际站:Chrysophanol
产品活性:Chrysophanol (Chrysophanic acid) 是一种天然蒽醌,抑制EGF-诱导的 EGFR 磷酸化,且抑制 AKT 和 mTOR/p70S6K 激活。
研究领域:JAK/STAT Signaling | Protein Tyrosine Kinase/RTK
作用靶点:EGFR
In Vitro: Chrysophanol (Chrysophanic Acid) blocks proliferation of colon cancer cells by inhibiting EGFR/mTOR pathway. Chrysophanol, a natural anthraquinone, has anticancer activity in EGFR-overexpressing SNU-C5 human colon cancer cells. Chrysophanol treatment in SNU-C5 cells inhibits EGF-induced phosphorylation of EGFR and suppresses activation of downstream signaling molecules, such as AKT, extracellular signal-regulated kinase (ERK) and the mammalian target of Rapamycin (mTOR)/ribosomal protein S6 kinase (p70S6K). Chrysophanol (80 and 120 μM) significantly blocks cell proliferation when combined with the mTOR inhibitor, Rapamycin. Chrysophanol inhibits EGF-induced phosphorylation of EGFR and suppresses activation of AKT and mTOR/p70S6K, and significantly blocks cell proliferation. Chrysophanol dose dependently decreases CCK-8 and the viability of EGFR-overexpressing SNU-C5 cells. Chrysophanol treatment dose-dependently decreases EGF induced phosphorylation of EGFR at Tyr1068. Chrysophanol (80 and 120 μM) reduces the phosphorylation levels of mTOR at Ser2448. Chrysophanol (80 and 120 μM) also decreases the phosphorylation levels of p70S6K at Thr389. Chrysophanol inhibits EGF-induced EGFR activation and suppresses activation of the downstream signaling molecules, AKT and mTOR/p70S6K. Chrysophanol (CA) inhibits lipid accumulation in 3T3-L1 adipocytes. Chrysophanol down-regulates adipogenic factors in 3T3-L1 adipocytes. Chrysophanol induces thermogenic factors in primary cultured brown adipocytes. Chrysophanol suppresses adipogenesis and induces thermogenesis via activation of AMPK pathway.
In Vivo: Chrysophanol (CA) improves HFD-induced obesity in C57BL/6 Mice. The in vivo performance of Chrysophanol is performed in male C57BL/6J mice to determine the efficacy of administered Chrysophanol. Mice fed the HFD gained significantly more weight than those fed the standard diet mice. On the other hand, weight gain of Chrysophanol group is significantly less than with the untreated HFD. Mice in the HFD-group gained 23.92 ± 1.74 g of weight, while those in the Chrysophanol group gained 16.72±2 g of weight after 16 weeks.
相关产品:Natural Product Library Plus | Bioactive Compound Library Plus | Immunology/Inflammation Compound Library | JAK/STAT Compound Library | Kinase Inhibitor Library | Protein Tyrosine Kinase Compound Library | Natural Product Library | Anti-Cancer Compound Library | Differentiation Inducing Compound Library | Traditional Chinese Medicine Monomer Library | Anti-Hepatitis C Virus Compound Library | Anti-Lung Cancer Compound Library | Anti-Pancreatic Cancer Compound Library | Gefitinib | Trastuzumab | Erlotinib | Cetuximab | AG490 | Genistein | AG-1478 | Pertuzumab | BI-4020 | NSC 228155 | Pelitinib | Mubritinib | TX1-85-1 | AZ7550 hydrochloride | Butein | PD168393 | AEE788 | Canertinib dihydrochloride | Daphnetin | EGFR-IN-7 | PD153035 | Tyrphostin 23 | BMS-599626 Hydrochloride | Trastuzumab emtansine | Falnidamol | Lavendustin A
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文献和实验与性质 1.大黄素(Emodin):橙黄色长针晶(丙酮中结晶为橙色,甲醇中结晶为黄色),mp256-257℃。几不溶于水,对于下列溶剂的溶介度分别为:四氯化碳0.01%,氯仿0.0718%,二硫化碳0.009%,乙醚0.14%,苯0.0415。易溶于乙醇,可溶于氨水,碳酸钠和氢氧化钠水溶液。 2.大黄酚(Chrysophanol):金黄色六角型片状结晶(丙酮中结晶)或针状结晶(乙醇中结晶)。mp 196℃,能升华。易溶于乙醚、氯仿、苯、冰乙酸、乙醇, 稍溶于甲醇,难溶于石油醚,不溶于水、碳酸
DNA Sequencing as a Tissue-Typing Tool
481 HLA-C 42 74 118 HLA- DPB1 77
我合成了好几对引物都因为产物的GC含量极高达74%,都没有成功,我又合成了一对引物,没有加酶切位点,想如果能P 出来就回收做摸板,大家请帮我看看,引物设计可行吗? 上游引物:5-ATGGCGGGCGTCTGCTCTCCACCTG-3 下游引物:5-CCACCTTGAAGTCATTCTCCAGGCGGC-3 如果 不行,请大家帮我设计一下引物,感激不尽!我已经做了快半年了.郁闷啊! 产物序列: 1 tgcagcggtt ctggatggcg ttattcgtac ttttgctgcg
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