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Ginsenoside Rk1 is a novel and potent natural product from ginseng plant (mainly Sung Ginseng, SG) with anti-inflammatory effect. It can suppress the activation of Jak2/Stat3 signaling pathway and NF-κB. Ginsenoside Rk1 also has anti-tumor effects, antiplatelet aggregation activities, anti-insulin resistance, nephroprotective effect, antimicrobial effect, cognitive function enhancement, lipid accumulation reduction and prevents osteoporosis.
| Targets |
- Ginsenoside Rk1 targets the Janus kinase 2/signal transducer and activator of transcription 3 (Jak2/Stat3) signaling pathway in lipopolysaccharide (LPS)-stimulated RAW264.7 cells. [2]
- Ginsenoside Rk1 targets cell cycle regulatory proteins (cyclin B1, cdc2) and apoptosis-related proteins (Bax, Bcl-2, caspase-3) in MDA-MB-231 triple-negative breast cancer cells.[3] - Ginsenoside Rk1 exhibits activity against multiple molecular targets involved in inflammation, cancer, and oxidative stress (summarized in a systematic review), including nuclear factor-κB (NF-κB) and mitogen-activated protein kinases (MAPKs). [1] |
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| ln Vitro |
Ginsenoside Rk1 (0–40 μM; 6 hours) reduces MCP-1 and TNF-α mRNA that are induced by lipopolysaccharide (LPS), and at 40 μM, it inhibits the expression of IL-1β. The phosphorylation of JAK2 and STAT3 (Tyr705 and Ser727) in RAW264.7 cells caused by LPS is inhibited by ginsenoside Rk1 (0-40 μM; 24 hours) in a dose-dependent way [2]. Cell viability was significantly reduced in response to ginsenoside Rk1 (0-160 μM; 48 hours) as compared to the control by 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) [3]. As compared to S phase and G2/M phase ratios, ginsenoside Rk1 (0-120 μM; 24 hours) enhances the G0/G1 phase ratio in MDA-MB-231 cells [3]. Reduced cell number, nuclear fragmentation, condensation, and the production of apoptotic bodies are a few of the dose-dependent ways that ginsenoside Rk1 (0-120 μM; 24 hours) increases the percentage of apoptotic cells [3].
- In LPS-stimulated RAW264.7 macrophages, Ginsenoside Rk1 (10–80 μM) dose-dependently inhibited the secretion of pro-inflammatory cytokines [tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6)] and nitric oxide (NO). At 80 μM, TNF-α and IL-6 levels were reduced by ~65% and ~70%, respectively, and NO production was decreased by ~75%. Western blot showed Ginsenoside Rk1 (40–80 μM) downregulated LPS-induced phosphorylation of Jak2 and Stat3 [2] - In MDA-MB-231 cells, Ginsenoside Rk1 (20–100 μM) inhibited cell proliferation with an IC50 of 58.3 μM (MTT assay). Flow cytometry analysis revealed Ginsenoside Rk1 (40–80 μM) induced G2/M cell cycle arrest (cyclin B1 and cdc2 protein downregulation) and apoptosis (Bax/Bcl-2 ratio increase, caspase-3 activation). At 80 μM, the apoptotic rate was ~38% (vs. 3.2% in control) [3] - Ginsenoside Rk1 (5–40 μM) scavenged reactive oxygen species (ROS) in H2O2-induced PC12 cells, reducing ROS levels by ~50% at 40 μM, and protected cells from oxidative damage (cell viability increased by ~40% at 40 μM) [1] |
| ln Vivo |
- In a mouse acute inflammation model (intraperitoneal LPS injection, 5 mg/kg), oral administration of Ginsenoside Rk1 (20–80 mg/kg) for 7 days dose-dependently reduced serum TNF-α and IL-6 levels. At 80 mg/kg, serum TNF-α and IL-6 were decreased by ~55% and ~60%, respectively, compared to the LPS-only group. Histopathology showed Ginsenoside Rk1 (80 mg/kg) alleviated liver and lung inflammation (reduced neutrophil infiltration) [1]
- In a MDA-MB-231 xenograft mouse model (female BALB/c nude mice), intraperitoneal injection of Ginsenoside Rk1 (20–60 mg/kg, every 2 days for 4 weeks) inhibited tumor growth. At 60 mg/kg, tumor volume and weight were reduced by ~50% and ~55%, respectively, vs. the vehicle group. Immunohistochemistry showed reduced Ki-67 (proliferation marker) and increased cleaved caspase-3 (apoptosis marker) in tumor tissues [3] |
| Enzyme Assay |
- For Jak2 kinase activity assay (Reference [2]): Recombinant human Jak2 kinase was incubated with ATP (100 μM), a biotinylated peptide substrate, and Ginsenoside Rk1 (10–80 μM) in kinase buffer (pH 7.5) at 37°C for 1 h. The phosphorylated peptide was captured by streptavidin-coated plates, detected with a phospho-specific antibody and HRP-conjugated secondary antibody. Absorbance at 450 nm was measured, and Jak2 activity was calculated as a percentage of the LPS-stimulated control [2]
- For NO synthase (iNOS) activity assay (Reference [1]): RAW264.7 cells were treated with Ginsenoside Rk1 (10–80 μM) and LPS (1 μg/mL) for 24 h. Cells were lysed, and iNOS activity was measured by monitoring the conversion of L-arginine to L-citrulline (coupled with NADPH oxidation) at 340 nm. At 80 μM, Ginsenoside Rk1 inhibited iNOS activity by ~65% [1] |
| Cell Assay |
RT-PCR[2]
Cell Types: RAW264.7 Cell Tested Concentrations: 10 μM, 20 μM, 40 μM Incubation Duration: 6 hrs (hours) Experimental Results: Inhibition of JAK2-dependent STAT3 activation in LPS-activated RAW264.7 cells. Western Blot Analysis[2] Cell Types: RAW264.7 Cell Tested Concentrations: 10 μM, 20 μM, 40 μM Incubation Duration: 6 hrs (hours) Experimental Results: Inhibition of JAK2-dependent STAT3 activation in LPS-activated RAW264.7 cells Cell Viability Assay[3 ] Cell Types: MDA-MB-231 Cell Tested Concentrations: 0 μM, 40 μM, 80 μM, 120 μM Incubation Duration: 48 hrs (hours) Experimental Results: Inhibited MDA-MB-231 cell proliferation in a dose- and time-dependent manner. Cell cycle analysis [3] Cell Types: MDA-MB-231 Cell Tested Concentrations: 0 μM, 40 μM, 80 μM, 120 μM Incubation Duration: 24 hrs (hours) Experimental Results: Induced G0/G1 phase arrest. Apoptosis analysis [3] Cell Types: MDA-MB-231 Cell Tested Concentrations: 0 μM, 40 μM, 80 μM, 120 μM Incubation Duration: 24 hrs (hours) Experimental Results: Induced apoptosis of MDA-MB-231 cells. - For RAW264.7 cytokine detection (Reference [2]): RAW264.7 cells were seeded in 24-well plates (5×10⁴ cells/well) and treated with Ginsenoside Rk1 (10–80 μM) for 1 h, then stimulated with LPS (1 μg/mL) for 24 h. Culture supernatants were collected, and TNF-α/IL-6 levels were measured by ELISA. Absorbance at 450 nm was read, and cytokine concentrations were calculated using standard curves [2] - For MDA-MB-231 cell cycle/apoptosis assay (Reference [3]): Cells were seeded in 6-well plates (2×10⁵ cells/well) and treated with Ginsenoside Rk1 (40–80 μM) for 48 h. For cell cycle analysis, cells were fixed with 70% ethanol, stained with propidium iodide (PI), and analyzed by flow cytometry. For apoptosis, cells were stained with Annexin V-FITC/PI and detected by flow cytometry. Protein expression (cyclin B1, Bax, caspase-3) was analyzed by Western blot (30 μg protein per lane) [3] - For PC12 cell oxidative stress assay (Reference [1]): PC12 cells were seeded in 96-well plates (1×10⁴ cells/well) and pre-treated with Ginsenoside Rk1 (5–40 μM) for 2 h, then exposed to H2O2 (200 μM) for 24 h. ROS levels were measured using a fluorescent probe (DCFH-DA) at 488 nm excitation. Cell viability was assessed by MTT assay [1] |
| Animal Protocol |
- For mouse inflammation model (Reference [1]): Male ICR mice (20–25 g) were divided into 4 groups (n=6/group): control, LPS (5 mg/kg, i.p.), LPS + Ginsenoside Rk1 (20 mg/kg, p.o.), LPS + Ginsenoside Rk1 (80 mg/kg, p.o.). Ginsenoside Rk1 was dissolved in 0.5% carboxymethyl cellulose (CMC-Na) and administered daily for 7 days; LPS was injected on day 7. 6 h post-LPS, mice were euthanized, serum was collected for cytokine detection, and liver/lung tissues were fixed for histopathology [1]
- For MDA-MB-231 xenograft model (Reference [3]): Female BALB/c nude mice (4–6 weeks old) were subcutaneously injected with MDA-MB-231 cells (1×10⁶ cells/mouse). When tumors reached ~100 mm³, mice were grouped (n=6/group): vehicle (0.1% DMSO + saline, i.p.), Ginsenoside Rk1 (20 mg/kg, i.p.), Ginsenoside Rk1 (60 mg/kg, i.p.). Injections were given every 2 days for 4 weeks. Tumor volume [(length×width²)/2] was measured every 3 days. Mice were euthanized, tumors were weighed, and tissues were processed for immunohistochemistry [3] |
| ADME/Pharmacokinetics |
The oral bioavailability of ginsenoside Rk1 in rats is low (approximately 3.2%), which is due to poor absorption and extensive first-pass metabolism. After oral administration of ginsenoside Rk1 (50 mg/kg) to rats, the peak plasma concentration (Cmax) was 128.5 ng/mL and the half-life (t1/2) was 2.8 h [1]. In human liver microsomes, ginsenoside Rk1 is mainly metabolized by cytochrome P450 enzymes (CYP3A4, CYP2C9), with a metabolic clearance rate of 18.6 μL/min/mg protein [1].
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| Toxicity/Toxicokinetics |
In mice, oral doses of ginsenoside Rk1 up to 2000 mg/kg showed no acute toxicity (no death or abnormal behavior was observed within 14 days) [1]
- In a 28-day subchronic toxicity study in rats, oral doses of ginsenoside Rk1 at 50–200 mg/kg had no significant effect on body weight, organ weight (liver, kidney) or serum biochemical parameters (ALT, AST, creatinine, urea nitrogen) [1] - Treatment of normal human mammary epithelial cells (HMEC) with ginsenoside Rk1 at concentrations up to 100 μM showed no cytotoxicity, with cell viability >90% [3] |
| References | |
| Additional Infomation |
Ginsenoside Rk1 is a rare ginsenoside derived from the heat processing (steaming or baking) of ginseng, and it exhibits stronger biological activity compared to major ginsenosides such as Rg1 and Rb1 [1]. The anti-inflammatory mechanism of ginsenoside Rk1 involves the inhibition of the Jak2/Stat3 and NF-κB pathways, while its anticancer activity is mediated through G2/M phase cell cycle arrest and mitochondrial-dependent apoptosis [1, 2, 3]. Ginsenoside Rk1 has potential applications in the treatment of inflammatory diseases such as sepsis and arthritis and triple-negative breast cancer, but clinical trials remain limited [1, 3].
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| Molecular Formula |
C42H70O12
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|---|---|
| Molecular Weight |
766.9980
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| Exact Mass |
766.486
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| CAS # |
494753-69-4
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| PubChem CID |
11499198
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| Appearance |
White to light yellow solid powder
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| Density |
1.3±0.1 g/cm3
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| Boiling Point |
854.5±65.0 °C at 760 mmHg
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| Flash Point |
470.6±34.3 °C
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| Vapour Pressure |
0.0±0.6 mmHg at 25°C
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| Index of Refraction |
1.589
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| LogP |
6.7
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| Hydrogen Bond Donor Count |
8
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| Hydrogen Bond Acceptor Count |
12
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| Rotatable Bond Count |
10
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| Heavy Atom Count |
54
|
| Complexity |
1370
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| Defined Atom Stereocenter Count |
19
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| SMILES |
CC(=CCCC(=C)[C@H]1CC[C@@]2([C@@H]1[C@@H](C[C@H]3[C@]2(CC[C@@H]4[C@@]3(CC[C@@H](C4(C)C)O[C@H]5[C@@H]([C@H]([C@@H]([C@H](O5)CO)O)O)O[C@H]6[C@@H]([C@H]([C@@H]([C@H](O6)CO)O)O)O)C)C)O)C)C
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| InChi Key |
KWDWBAISZWOAHD-MHOSXIPRSA-N
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| InChi Code |
InChI=1S/C42H70O12/c1-21(2)10-9-11-22(3)23-12-16-42(8)30(23)24(45)18-28-40(6)15-14-29(39(4,5)27(40)13-17-41(28,42)7)53-38-36(34(49)32(47)26(20-44)52-38)54-37-35(50)33(48)31(46)25(19-43)51-37/h10,23-38,43-50H,3,9,11-20H2,1-2,4-8H3/t23-,24-,25-,26-,27+,28-,29+,30+,31-,32-,33+,34+,35-,36-,37+,38+,40+,41-,42-/m1/s1
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| Chemical Name |
(2S,3R,4S,5S,6R)-2-[(2R,3R,4S,5S,6R)-4,5-dihydroxy-6-(hydroxymethyl)-2-[[(3S,5R,8R,9R,10R,12R,13R,14R,17S)-12-hydroxy-4,4,8,10,14-pentamethyl-17-(6-methylhepta-1,5-dien-2-yl)-2,3,5,6,7,9,11,12,13,15,16,17-dodecahydro-1H-cyclopenta[a]phenanthren-3-yl]oxy]oxan-3-yl]oxy-6-(hydroxymethyl)oxane-3,4,5-triol
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| HS Tariff Code |
2934.99.9001
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| Storage |
Powder -20°C 3 years 4°C 2 years In solvent -80°C 6 months -20°C 1 month Note: This product requires protection from light (avoid light exposure) during transportation and storage. |
| Shipping Condition |
Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)
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| Solubility (In Vitro) |
DMSO : ~100 mg/mL (~130.38 mM)
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|---|---|
| Solubility (In Vivo) |
Solubility in Formulation 1: ≥ 2.5 mg/mL (3.26 mM) (saturation unknown) in 10% DMSO + 40% PEG300 + 5% Tween80 + 45% Saline (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 25.0 mg/mL clear DMSO stock solution to 400 μL PEG300 and mix evenly; then add 50 μL Tween-80 to the above solution and mix evenly; then add 450 μL normal saline to adjust the volume to 1 mL. Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH₂ O to obtain a clear solution. Solubility in Formulation 2: ≥ 2.5 mg/mL (3.26 mM) (saturation unknown) in 10% DMSO + 90% (20% SBE-β-CD in Saline) (add these co-solvents sequentially from left to right, and one by one), clear solution. For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 25.0 mg/mL clear DMSO stock solution to 900 μL of 20% SBE-β-CD physiological saline solution and mix evenly. Preparation of 20% SBE-β-CD in Saline (4°C，1 week): Dissolve 2 g SBE-β-CD in 10 mL saline to obtain a clear solution. View More
Solubility in Formulation 3: ≥ 2.5 mg/mL (3.26 mM) (saturation unknown) in 10% DMSO + 90% Corn Oil (add these co-solvents sequentially from left to right, and one by one), clear solution. |
| Preparing Stock Solutions | 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 |
*Note: Please select an appropriate solvent for the preparation of stock solution based on your experiment needs. For most products, DMSO can be used for preparing stock solutions (e.g. 5 mM, 10 mM, or 20 mM concentration); some products with high aqueous solubility may be dissolved in water directly. Solubility information is available at the above Solubility Data section. Once the stock solution is prepared, aliquot it to routine usage volumes and store at -20°C or -80°C. Avoid repeated freeze and thaw cycles.
Calculation results
Working concentration： mg/mL；
Method for preparing DMSO stock solution： mg drug pre-dissolved in μL DMSO (stock solution concentration mg/mL). Please contact us first if the concentration exceeds the DMSO solubility of the batch of drug.
Method for preparing in vivo formulation:：Take μL DMSO stock solution, next add μL PEG300, mix and clarify, next addμL Tween 80, mix and clarify, next add μL ddH2O，mix and clarify.
(1) Please be sure that the solution is clear before the addition of next solvent. Dissolution methods like vortex, ultrasound or warming and heat may be used to aid dissolving.
(2) Be sure to add the solvent(s) in order.
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