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Notoginsenoside R2
ChemFaces products have been cited in many studies from excellent and top scientific journals
Product Name Notoginsenoside R2
Price: $158 / 20mg
CAS No.: 80418-25-3
Catalog No.: CFN92364
Molecular Formula: C41H70O13
Molecular Weight: 771.0 g/mol
Purity: >=98%
Type of Compound: Triterpenoids
Physical Desc.: Powder
Source: The roots of Panax notoginseng (Burk.)F.H.Chen
Solvent: DMSO, Pyridine, Methanol, Ethanol, etc.
Download: COA    MSDS    SDF    Manual
Similar structural: Comparison (Web)  (SDF)
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Related Screening Libraries
Size /Price /Stock 10 mM * 100 uL in DMSO / Inquiry / In-stock
10 mM * 1 mL in DMSO / Inquiry / In-stock
Related Libraries
Biological Activity
Description: Notoginsenoside R2 has neuroprotection against 6-OHDA-induced neurotoxicity, is associated with Notoginsenoside R2-mediated P90RSK and Nrf2 activation through MEK1/2-ERK1/2 pathways.
Targets: Nrf2 | MEK | ERK | P90RSK
Notoginsenoside R2 Description
Source: The roots of Panax notoginseng (Burk.)F.H.Chen
Solvent: DMSO, Pyridine, Methanol, Ethanol, etc.
Storage: 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

After receiving: 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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Recently, ChemFaces products have been cited in many studies from excellent and top scientific journals

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
Calculate Dilution Ratios(Only for Reference)
1 mg 5 mg 10 mg 20 mg 25 mg
1 mM 1.297 mL 6.4851 mL 12.9702 mL 25.9403 mL 32.4254 mL
5 mM 0.2594 mL 1.297 mL 2.594 mL 5.1881 mL 6.4851 mL
10 mM 0.1297 mL 0.6485 mL 1.297 mL 2.594 mL 3.2425 mL
50 mM 0.0259 mL 0.1297 mL 0.2594 mL 0.5188 mL 0.6485 mL
100 mM 0.013 mL 0.0649 mL 0.1297 mL 0.2594 mL 0.3243 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.
Protocol
Kinase Assay:
Evid Based Complement Alternat Med. 2013;2013:971712.
P90RSK and Nrf2 Activation via MEK1/2-ERK1/2 Pathways Mediated by Notoginsenoside R2 to Prevent 6-Hydroxydopamine-Induced Apoptotic Death in SH-SY5Y Cells.[Pubmed: 24159358]
6-Hydroxydopamine (6-OHDA) is known to contribute to neuronal death in Parkinson's disease.
METHODS AND RESULTS:
In this study, we found that the preincubation of SH-SY5Y cells for 24 h with 20  μ M Notoginsenoside R2 (NGR2), which is a newly isolated notoginsenoside from Panax notoginseng, showed neuroprotective effects against 6-OHDA-induced oxidative stress and apoptosis. NGR2 incubation successively resulted in the activation of P90RSK, inactivation of BAD, and inhibition of 6-OHDA-induced mitochondrial membrane depolarization, thus preventing the mitochondrial apoptosis pathway. NGR2 incubation also led to the activation of Nrf2 and subsequent activity enhancement of phase II detoxifying enzymes, thus suppressing 6-OHDA-induced oxidative stress, and these effects could be removed by Nrf2 siRNA. We also found that the upstream activators of P90RSK and Nrf2 were the MEK1/2-ERK1/2 pathways but not the JNK, P38, or PI3K/Akt pathways. Interestingly, NGR2 incubation could also activate MEK1/2 and ERK1/2. Most importantly, NGR2-mediated P90RSK and Nrf2 activation, respective downstream target activation, and neuroprotection were reversed by the genetic silencing of MEK1/2 and ERK1/2 by using siRNA and PD98059 application.
CONCLUSIONS:
These results suggested that the neuroprotection elicited by NGR2 against 6-OHDA-induced neurotoxicity was associated with NGR2-mediated P90RSK and Nrf2 activation through MEK1/2-ERK1/2 pathways.
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