Ginsenoside Rg3(S-Form)
APC-1361
Ginsenoside Rg3(S-Form)
Cat. No.
APC-1361
CAS No.
14197-60-5
MF
C42H72O13
MW
785.0133
Ginsenoside Rg3(S-Form) is the main component of Panax ginseng C. A. Meyer. It inhibits Na+ and hKv1.4channel, and also inhibits Aβ levels, NF-κB activity, and COX-2 expression.
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Technical Data
Description
Storage and Shipping
References
Product Name
CAS No.
14197-60-5
MF
C42H72O13
MW
785.0133
Specification
98%
Research Area
Antitumor, Anti-angiogenic,Antioxidant
Description
Ginsenoside Rg3(S-Form) is the main component of Panax ginseng C. A. Meyer. It inhibits Na+ and hKv1.4channel, and also inhibits Aβ levels, NF-κB activity, and COX-2 expression. Packing: 10mg, 20mg, 50mg, 100mg, 500mg, 1g, 5g, 10g Availability: In stock
Documents
Certificate of Analysis (COA), Specification Sheet, HPLC, 1HNMR, 13CNMR, IR, MS, Safety Data Sheet (SDS/MSDS) etc.
Storage and Shipping
Store under frozen or refrigerated conditions, keep away from strong light and heat.
References
[1]. Kim JH, et al. A role for the carbohydrate portion of ginsenoside Rg3 in Na+ channel inhibition. Mol Cells. 2005 Feb 28;19(1):137-42.
[2]. Lee JH, et al. Ginsenoside Rg3 inhibits human Kv1.4 channel currents by interacting with the Lys531 residue. Mol Pharmacol. 2008 Mar;73(3):619-26.
[3]. Lee IS, et al. Anti-Inflammatory Effects of Ginsenoside Rg3 via NF-κB Pathway in A549 Cells and Human Asthmatic Lung Tissue. J Immunol Res. 2016;2016:7521601.
[2]. Lee JH, et al. Ginsenoside Rg3 inhibits human Kv1.4 channel currents by interacting with the Lys531 residue. Mol Pharmacol. 2008 Mar;73(3):619-26.
[3]. Lee IS, et al. Anti-Inflammatory Effects of Ginsenoside Rg3 via NF-κB Pathway in A549 Cells and Human Asthmatic Lung Tissue. J Immunol Res. 2016;2016:7521601.
Disclaimer
This product is intended solely for scientific research or regulatory filing purposes. We do not provide products or services to individuals, please strictly comply with all applicable laws, regulations, and the committed use. Use for any other purpose is strictly prohibited.
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