Ginsenoside Rk3

Ginsenoside Rk3
Product Name Ginsenoside Rk3
CAS No.: 364779-15-7
Catalog No.: CFN92593
Molecular Formula: C36H60O8
Molecular Weight: 620.9 g/mol
Purity: >=98%
Type of Compound: Triterpenoids
Physical Desc.: Powder
Targets: Bcl-2/Bax | Caspase | Akt | Nrf2 | HO-1 | MAPK | NF-κB
Source: The roots of Panax ginseng C. A. Mey.
Solvent: DMSO, Pyridine, Methanol, Ethanol, etc.
Price: $180/10mg
Ginsenoside Rk3 is often used as a major ingredient of the compound preparation for ischemic heart diseases, it could have a role in treating inflammatory diseases. Ginsenoside Rk3 significantly inhibits TNF-α-induced NF-κB transcriptional activity, with an IC50 of 14.24±1.30 μM in HepG2 cells.
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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

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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    Evid Based Complement Alternat Med. 2013;2013:690190.
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    Cardiac hypertrophy is a thickening of the heart muscle that is associated with cardiovascular diseases such as hypertension and myocardial infarction. It occurs initially as an adaptive process against increased workloads and often leads to sudden arrhythmic deaths. Studies suggest that the lethal arrhythmia is attributed to hypertrophy-induced destabilization of cardiac electrical activity, especially the prolongation of the action potential. The reduced activity of Ito is demonstrated to be responsible for the ionic mechanism of prolonged action potential duration and arrhythmogeneity. Isosteviol (STV), a derivative of stevioside, plays a protective role in a variety of stress-induced cardiac diseases.
    METHODS AND RESULTS:
    Here we report effects of STV on rat ISO-induced hypertrophic cardiomyocytes. STV alleviated ISO-induced hypertrophy of cardiomyocytes by decreasing cell area of hypertrophied cardiomyocytes. STV application prevented the prolongation of action potential which was prominent in hypertrophied cells.
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    The decrease and increase of current densities for Ito and ICaL observed in hypertrophied myocytes were both prevented by STV application. In addition, the results of qRT-PCR suggested that the changes of electrophysiological activity of Ito and ICaL are correlated to the alterations of the mRNA transcription level.
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