[CAS NO. 494753-69-4]  Ginsenoside Rk1

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PRODUCTS SPECIFICATIONS [494753-69-4]

Distributor
Catalog
HY-N2515
Brand
MCE
CAS
494753-69-4

DESCRIPTION [494753-69-4]

Overview

MDLMFCD28124355
Molecular Weight767.00
Molecular FormulaC42H70O12
SMILESC[C@]12[C@@](C[C@@H](O)[C@@]3([H])[C@]2(CC[C@@H]3C(CC/C=C(C)/C)=C)C)([H])[C@@]4([C@@](C(C)([C@@H](O[C@@]5([H])[C@@H]([C@H]([C@H](O)[C@@H](CO)O5)O)O[C@]6([H])O[C@@H]([C@@H](O)[C@H](O)[C@H]6O)CO)CC4)C)([H])CC1)C

For research use only. We do not sell to patients.

1 Publications Citing Use of MCE


Summary

Ginsenoside Rk1 is a unique component created by processing the ginseng plant (mainly Sung Ginseng, SG) at high temperatures [1] . Ginsenoside Rk1 has anti-inflammatory effect, suppresses the activation of Jak2/Stat3 signaling pathway and NF-κB [2] . Ginsenoside Rk1 has anti-tumor effect, antiplatelet aggregation activities, anti-insulin resistance, nephroprotective effect, antimicrobial effect, cognitive function enhancement, lipid accumulation reduction and prevents osteoporosis [1] . Ginsenoside Rk1 induces cell apoptosis by triggering intracellular reactive oxygen species ( ROS ) generation and blocking PI3K/Akt pathway [3] .


In Vitro

Ginsenoside Rk1 (0-40 μM; 6 hours) inhibits MCP-1 and TNF-α mRNA induced by lipopolysaccharide (LPS), expression of IL-1β is inhibited at 40 μM [2] .
Ginsenoside Rk1 (0-40 μM; 24 hours) inhibits phosphorylation of JAK2 and STAT3 (Tyr705 and Ser727) in LPS-induced RAW264.7 cells in a dose-dependent manner [2] .
Ginsenoside Rk1 (0-160 μM; 48 hours) results in cell viability significant decrease 75.52 ± 2.51% (40 μM), 52.72 ± 2.54% (80 μM), 17.41 ± 2.94% (120 μM)and 12.63 ± 3.24% (160 μM) compared with control [3] .
Ginsenoside Rk1 (0-120 μM; 24 hours) increases G0/G1 phase proportion accompanied with S and G2/M phase proportion decrease in MDA-MB-231 cells [3] .
Ginsenoside Rk1 (0-120 μM; 24 hours) promotes the percentage of apoptotic cells in a dose-dependent manner, exhibits to reduction of cell number with nucleus fragmentation, condensation and apoptotic body formation [3] .

MCE has not independently confirmed the accuracy of these methods. They are for reference only.

RT-PCR [2]

Cell Line: RAW264.7 cells
Concentration: 10 μM, 20 μM, 40 μM
Incubation Time: 6 hours
Result: Inhibited JAK2-dependent STAT3 activation in LPS-activated RAW264.7 cells.

Western Blot Analysis [2]

Cell Line: RAW264.7 cells
Concentration: 10 μM, 20 μM, 40 μM
Incubation Time: 6 hours
Result: Inhibited JAK2-dependent STAT3 activation in LPS-activated RAW264.7 cells

Cell Viability Assay [3]

Cell Line: MDA-MB-231 cells
Concentration: 0 μM, 40 μM, 80 μM, 120 μM
Incubation Time: 48 hours
Result: Inhibited MDA-MB-231 cells proliferation in a dose- and time-dependent manner.

Cell Cycle Analysis [3]

Cell Line: MDA-MB-231 cells
Concentration: 0 μM, 40 μM, 80 μM, 120 μM
Incubation Time: 24 hours
Result: Induced G0/G1 phase arrest.

Apoptosis Analysis [3]

Cell Line: MDA-MB-231 cells
Concentration: 0 μM, 40 μM, 80 μM, 120 μM
Incubation Time: 24 hours
Result: Induced apoptosis in MDA-MB-231 cells.

Appearance

Solid



Shipping

Room temperature in continental US; may vary elsewhere.


Storage

-20°C, protect from light

* In solvent : -80°C, 6 months; -20°C, 1 month (protect from light)


Solvent & Solubility

In Vitro:

DMSO : 100 mg/mL ( 130.38 mM ; Need ultrasonic)

Preparing
Stock Solutions
Concentration Solvent Mass 1 mg 5 mg 10 mg
1 mM 1.3038 mL 6.5189 mL 13.0378 mL
5 mM 0.2608 mL 1.3038 mL 2.6076 mL
10 mM 0.1304 mL 0.6519 mL 1.3038 mL
* Please refer to the solubility information to select the appropriate solvent.
In Vivo:
  • 1.

    Add each solvent one by one: 10% DMSO >> 40% PEG300 >> 5% Tween-80 >> 45% saline

    Solubility: ≥ 2.5 mg/mL (3.26 mM); Clear solution

  • 2.

    Add each solvent one by one: 10% DMSO >> 90% (20% SBE-β-CD in saline)

    Solubility: ≥ 2.5 mg/mL (3.26 mM); Clear solution

  • 3.

    Add each solvent one by one: 10% DMSO >> 90% corn oil

    Solubility: ≥ 2.5 mg/mL (3.26 mM); Clear solution

* All of the co-solvents are available by MCE.