Ginsenoside CK
(Synonyms: 20(S)-人参皂苷 C-K ) 目录号 : GC20007
A metabolite of ginsenoside Rb1 with diverse biological activity
Cas No.:39262-14-1
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
- View current batch:
| Cas No. | 39262-14-1 | SDF | |
| 别名 | 20(S)-人参皂苷 C-K | ||
| 分子式 | C36H62O8 | 分子量 | 622.87 |
| 溶解度 | 储存条件 | RT | |
| General tips | 请根据产品在不同溶剂中的溶解度选择合适的溶剂配制储备液；一旦配成溶液，请分装保存，避免反复冻融造成的产品失效。 储备液的保存方式和期限：-80°C 储存时，请在 6 个月内使用，-20°C 储存时，请在 1 个月内使用。 为了提高溶解度，请将管子加热至37℃，然后在超声波浴中震荡一段时间。 |
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| Shipping Condition | 评估样品解决方案：配备蓝冰进行发货。所有其他可用尺寸：配备RT，或根据请求配备蓝冰。 | ||
| 制备储备液 | |||
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1 mg | 5 mg | 10 mg |
| 1 mM | 1.6055 mL | 8.0274 mL | 16.0547 mL |
| 5 mM | 0.3211 mL | 1.6055 mL | 3.2109 mL |
| 10 mM | 0.1605 mL | 0.8027 mL | 1.6055 mL |
| 第一步：请输入基本实验信息（考虑到实验过程中的损耗，建议多配一只动物的药量） | ||||||||||
| 给药剂量 | mg/kg |  |
动物平均体重 | g | |
每只动物给药体积 | ul | |
动物数量 | 只 |
| 第二步：请输入动物体内配方组成（配方适用于不溶于水的药物；不同批次药物配方比例不同，请联系GLPBIO为您提供正确的澄清溶液配方） | ||||||||||
| % DMSO % % Tween 80 % saline | ||||||||||
| 计算重置 | ||||||||||
计算结果:
工作液浓度： mg/ml；
DMSO母液配制方法： mg 药物溶于 μL DMSO溶液（母液浓度 mg/mL，
体内配方配制方法：取 μL DMSO母液，加入 μL PEG300，混匀澄清后加入μL Tween 80，混匀澄清后加入 μL saline，混匀澄清。
1. 首先保证母液是澄清的；
2.
一定要按照顺序依次将溶剂加入，进行下一步操作之前必须保证上一步操作得到的是澄清的溶液，可采用涡旋、超声或水浴加热等物理方法助溶。
3. 以上所有助溶剂都可在 GlpBio 网站选购。
A derivant of Ginsenoside CK and its inhibitory effect on hepatocellular carcinoma
Life Sci 2022 Sep 1;304:120698.PMID:35690105DOI:10.1016/j.lfs.2022.120698.
Epidemiological studies have shown that hepatocellular carcinoma (HCC) is a main cause of tumor death worldwide. Accumulating data indicate that Ginsenoside CK is an effective compound for preventing HCC growth and development. However, improvement of pharmaceutical effect of the Ginsenoside CK is still needed. In our study, we performed acetylation of Ginsenoside CK (CK-3) and investigated the antitumor effects of the derivative in vitro and in vivo. The cytotoxicity analysis revealed that compared with CK, CK-3 could inhibit the proliferation of multiple tumor cell lines at a lower concentration. Treating with CK-3 on HCC cells arrested cell cycle in G2/M phase and induced cell apoptosis through AO/EB staining, TUNEL analysis and flow cytometry. Meanwhile, CK-3 significantly inhibited tumor growth in an HCC xenograft model and showed no side effect on the function of the main organs. Mechanistically, whole transcriptome analysis revealed that the antitumor effect of CK-3 was involved in the Hippo signaling pathway. The immunoblotting and immunofluorescence results illustrated that CK-3 directly facilitated the phosphorylation of YAP1 and decreased the expression of the main transcription factor TEAD2 in HCC cell lines and tumor tissue sections. Collectively, our results demostrate the formation of a new derivative of Ginsenoside CK and its regulatory mechanism in HCC, which could activate the Hippo-YAP1-TEAD2 signaling pathway to regulate HCC progression. This research could provide a new direction for traditional Chinese medicine in the therapy of tumors.
Ginsenoside CK induces apoptosis in triple-negative breast cancer cells by targeting glutamine metabolism
Biochem Pharmacol 2022 Aug;202:115101.PMID:35618001DOI:10.1016/j.bcp.2022.115101.
Breast cancer (BC) has replaced lung cancer as the most common cancer worldwide. Ginsenoside CK (CK) can effectively inhibit triple-negative breast cancer (TNBC), the occurrence and development of which are associated with glutamine addiction. However, the connection between CK and glutamine metabolism in TNBC proliferation and the mechanism of cell death induction remains unclear. Here, we found that high glutamine-addicted TNBC cells were particularly sensitive to CK treatment. CK exerted antitumour activity against TNBC by suppressing glutamine consumption and glutamate production via downregulation of glutaminase 1 (GLS1) expression. CK treatment further decreased cellular ATP production, reduced the utilisation of amino acids associated with glutamine metabolism, and induced glutathione (GSH) depletion and reactive oxygen species (ROS) accumulation, consequently triggering apoptosis in TNBC. Furthermore, CK decreased GLS1 expression in SUM159 xenograft mouse mammary tumours and significantly inhibited tumour growth with few side effects. Together, our data provide a powerful theoretical basis for the application of CK as a glutamine metabolic inhibitor in TNBC treatment.
Production of Minor Ginsenoside CK from Major Ginsenosides by Biotransformation and Its Advances in Targeted Delivery to Tumor Tissues Using Nanoformulations
Nanomaterials (Basel) 2022 Sep 30;12(19):3427.PMID:36234555DOI:10.3390/nano12193427.
For over 2000 years, ginseng (roots of Panax ginseng C.A. Meyer) has been used as a traditional herbal medicine. Ginsenosides are bioactive compounds present in ginseng responsible for the pharmacological effects and curing various acute diseases as well as chronic diseases including cardiovascular disease, cancer and diabetes. Structurally, ginsenosides consist of a hydrophobic aglycone moiety fused with one to four hydrophilic glycoside moieties. Based on the position of sugar units and their abundance, ginsenosides are classified into major and minor ginsenosides. Despite the great potential of ginsenosides, major ginsenosides are poorly absorbed in the blood circulation, resulting in poor bioavailability. Interestingly, owing to their small molecular weight, minor ginsenosides exhibit good permeability across cell membranes and bioavailability. However, extremely small quantities of minor ginsenosides extracted from ginseng plants cannot fulfill the requirement of scientific and clinical studies. Therefore, the production of minor ginsenosides in mass production is a topic of interest. In addition, their poor solubility and lack of targetability to tumor tissues limits their application in cancer therapy. In this review, various methods used for the transformation of major ginsenosides to minor ginsenoside compound K (CK) are summarized. For the production of CK, various transformation methods apply to major ginsenosides. The challenges present in these transformations and future research directions for producing bulk quantities of minor ginsenosides are discussed. Furthermore, attention is also paid to the utilization of nanoformulation technology to improve the bioavailability of minor Ginsenoside CK.
Biotransformation of Ginsenoside Rb1 to Ginsenoside CK by Strain XD101: a Safe Bioconversion Strategy
Appl Biochem Biotechnol 2021 Jul;193(7):2110-2127.PMID:33629278DOI:10.1007/s12010-021-03485-0.
Ginsenoside Rb1 is the main predominant component in Panax species. In this study, an eco-friendly and convenient preparation method for Ginsenoside CK has been established, and five strains of β-glucosidase-producing microorganisms were screened out from the soil of a Panax notoginseng planting field using Esculin-R2A agar. Aspergillus niger XD101 showed that it has excellent biocatalytic activity for ginsenosides; one of the isolates can convert ginsenoside Rb1 to CK using extracellular enzyme from the mycelium. Mycelia of A. niger were cultivated in wheat bran media at 30 °C for 11 days. By the removal of mycelia from cultured broth, enzyme salt fractionation by ammonium sulfate (70%, v/v) precipitation, and dialysis, sequentially, crude enzyme preparations from fermentation liquid supernatant were obtained. The enzymatic transformed Rb1 as the following pathways: Rb1→Rd→F2→CK. The optimized reaction conditions are at reaction time of 72 h, in the range of pH 4-5, and temperature of 50-60 °C. Active minor ginsenosides can be obtained by a specific bioconversion via A. niger XD101 producing the ginsenoside-hydrolyzing β-glucosidase. In addition, the crude enzyme can be resulted in producing Ginsenoside CK via conversion of ginsenoside Rb1 at high conversion yield (94.4%). FDA generally regarded, A.niger as safe microorganism. Therefore, these results indicate that A. niger XD10 may provide an alternative method to prepare Ginsenoside CK without food safety issues in the pharmaceutical industry.
Ginsenoside CK Inhibits TGF- β-Induced Epithelial-Mesenchymal Transition in A549 Cell via SIRT1
Biomed Res Int 2021 Dec 12;2021:9140191.PMID:34934771DOI:10.1155/2021/9140191.
Ginsenoside CK is the main metabolite of protopanaxadiol saponins in intestinal bacteria. Previous studies have shown that Ginsenoside CK can affect many aspects of tumor development through a variety of mechanisms. However, few studies have reported the antimetastatic effects of Ginsenoside CK in non-small-cell lung cancer (NSCLC). In this study, we explored the effect of Ginsenoside CK on epithelial-mesenchymal transition (EMT) induced by TGF-β in A549 cells and the potential molecular mechanisms. Our data showed that Ginsenoside CK effectively prevented TGF-β-induced EMT, as indicated by the upregulation of E-cadherin and downregulation of vimentin. Furthermore, Ginsenoside CK inhibited the metastatic ability of A549 cells in the tail vein lung metastasis model of nude mice. Additionally, Ginsenoside CK decreased the expression of silent information regulator 2 homolog 1 (SIRT1) in the inhibition of EMT induced by TGF-β. Moreover, the antimetastatic effect of Ginsenoside CK was reversed by SIRT1 overexpression. Generally, our results indicated the antimetastatic effect and underlying mechanism of Ginsenoside CK on TGF-β-induced EMT in A549 cells, suggesting that Ginsenoside CK can be used as an effective antineoplastic agent.