Ginsenoside F4 has an IC50 value of 87.74 μM for suppressing JK cell proliferation[1]. In human tumor JK cells, ginsenoside F4 (8.15–130.38 μM) effectively provides dosage feeding by upregulating Bax expression and downregulating Bcl-2 expression [1]. Ginsenoside F4 (8.15–130.38 μM) exhibits anti-tumor action and promotes JK cell carcinoma in humans [1].

Ginsenoside F4 has an IC50 value of 87.74 μM for suppressing JK cell proliferation[1]. In human tumor JK cells, ginsenoside F4 (8.15–130.38 μM) effectively provides dosage feeding by upregulating Bax expression and downregulating Bcl-2 expression [1]. Ginsenoside F4 (8.15–130.38 μM) exhibits anti-tumor action and promotes JK cell carcinoma in humans [1].

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Ginsenoside F4 (GF4) inhibited the proliferation of human lymphocytoma Jurkat (JK) cells in a dose-dependent manner, with an IC₅₀ value of 87.74 μM. [1]
Treatment of JK cells with GF4 at concentrations of 65.19 μM and 130.38 μM for 72 hours induced cell apoptosis, with apoptosis rates of 23.95% and 68.80%, respectively, as determined by Annexin V-FITC/PI double staining and flow cytometry. [1]
Western blot analysis showed that treatment of JK cells with GF4 resulted in a gradual increase in the expression level of the pro-apoptotic protein Bax and a gradual decrease in the expression level of the anti-apoptotic protein Bcl-2, in a concentration-dependent manner. [1]

Ginsenoside F4 (GF4) inhibited interleukin-1β (IL-1β)-induced MMP-13 expression in human chondrosarcoma SW1353 cells in a concentration-dependent manner at non-cytotoxic concentrations (1-50 μM). At 10, 30, and 50 μM, the inhibition rates were 33.5%, 57.8%, and 90.0%, respectively. [2]
Ginsenoside F4 (GF4) (at 30 and 50 μM) strongly inhibited the activation (phosphorylation) of p38 MAPK in IL-1β-treated SW1353 cells, with inhibition rates of 86.6% and 100.0%, respectively. It did not affect the activation of ERK, JNK, or transcription factors such as NF-κB, AP-1, and STAT-1/-2 under the same conditions. [2]
Ginsenoside F4 (GF4) reduced glycosaminoglycan (GAG) release from interleukin-1α (IL-1α)-treated rabbit joint cartilage explants in culture. At concentrations of 2 μM and 10 μM, it inhibited GAG release by 18.0% and 25.2%, respectively, although these reductions were not statistically significant. [2]
Cell viability assays (MTT) confirmed that Ginsenoside F4 (GF4) was not cytotoxic to SW1353 cells at concentrations up to 50 μM. [2]

Western Blot Analysis[1]
Cell Types: Human Lymphocytoma JK cells
Tested Concentrations: 8.15 μM, 65.19 μM, 130.38 μM.
Incubation Duration:
Experimental Results: Bcl-2 protein level diminished and Bax level increased. This change is related to cell apoptosis.

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The anti-proliferative effect of Ginsenoside F4 (GF4) on human lymphocytoma Jurkat (JK) cells was assessed using the Cell Counting Kit-8 (CCK-8) assay. Cells were treated with various concentrations of GF4. After the treatment period, the CCK-8 reagent was added to the wells, and the plates were incubated. The absorbance was then measured at a specific wavelength to determine cell viability and calculate the IC₅₀ value. [1]
Cell apoptosis was detected using Annexin V-FITC/PI double staining followed by flow cytometry. JK cells were treated with GF4 at specified concentrations for 72 hours. After treatment, cells were harvested, washed, and resuspended in a binding buffer. Annexin V-FITC and propidium iodide (PI) were added to the cell suspension and incubated in the dark. The stained cells were then analyzed by flow cytometry to distinguish between viable cells (Annexin V⁻/PI⁻), early apoptotic cells (Annexin V⁺/PI⁻), and late apoptotic/necrotic cells (Annexin V⁺/PI⁺). The percentage of apoptotic cells was calculated. [1]
The effect of GF4 on the expression of apoptosis-related proteins (Bax and Bcl-2) was determined by Western blotting. JK cells were treated with different concentrations of GF4. After treatment, total cellular proteins were extracted. Equal amounts of protein samples were separated by SDS-PAGE and transferred onto a membrane. The membrane was blocked and then incubated with primary antibodies against Bax and Bcl-2, followed by incubation with appropriate secondary antibodies. Protein bands were visualized using a detection system, and their intensities were analyzed to assess changes in expression levels. [1]
SW1353 cells were cultured and maintained in Dulbecco's Modified Eagle Medium (DMEM) supplemented with fetal bovine serum (FBS), glutamine, and antibiotics. For MMP-13 induction experiments, cells were treated with IL-1β (10 ng/mL) in serum-free DMEM in the presence or absence of various concentrations of Ginsenoside F4 (GF4) for 24 hours. Test compounds were initially dissolved in dimethyl sulfoxide (DMSO) and diluted in serum-free medium, with the final DMSO concentration not exceeding 0.1% (v/v). After incubation, the culture media were collected to analyze MMP-13 protein levels by Western blotting. [2]
For Western blot analysis of MMP-13, proteins in the collected media were separated by SDS-PAGE, transferred onto a membrane, and probed with a specific anti-MMP-13 antibody. The protein bands were visualized using an enhanced chemiluminescence (ECL) detection system, and their densities were quantified using image analysis software. The expression level was normalized to a loading control. [2]
To investigate the signaling mechanism, SW1353 cells were pre-treated with or without Ginsenoside F4 (GF4) for a specified time before stimulation with IL-1β. Total cellular proteins or nuclear proteins were then extracted. The phosphorylation states of MAPKs (p38, ERK, JNK) and the levels/activation of transcription factors (NF-κB p65, c-Fos, c-Jun, STATs) were analyzed by Western blotting using specific antibodies. [2]
Cell viability was assessed using the MTT assay. After treatment with Ginsenoside F4 (GF4) and IL-1β for 24 hours, MTT reagent was added to the cells and incubated. The resulting formazan crystals were dissolved, and the absorbance was measured to determine cell viability relative to the control group. [2]

Articular cartilage explants were obtained from the femoral condyles of knee joints of male New Zealand white rabbits. The cartilage was cut into small fragments under sterile conditions. Approximately 30 mg of cartilage fragments were placed in each well of a 48-well plate and pre-cultured in DMEM containing 5% FBS for 1-2 days. The culture medium was then replaced with DMEM containing 1% FBS. The cartilage explants were treated with human IL-1α (10 ng/mL) to induce degradation, in the presence or absence of Ginsenoside F4 (GF4) at concentrations of 2 μM and 10 μM. The culture was maintained for 3 days. The supernatant was collected, and the amount of glycosaminoglycan (GAG) released into the medium was quantified using a dimethylmethylene blue (DMMB)-based assay kit according to the manufacturer's instructions. [2]

[1]. The apoptosis-inducing effect of ginsenoside F4 from steamed notoginseng on human lymphocytoma JK cells. Nat Prod Res. 2013;27(24):2351-4.

[2]. Ginsenosides from Korean red ginseng inhibit matrix metalloproteinase-13 expression in articular chondrocytes and prevent cartilage degradation. Eur J Pharmacol. 2014 Feb 5;724:145-51.

Ginsenoside F4 (GF4) is a component isolated from steamed Panax notoginseng (the root of ginseng). [1] Studies have shown that the mechanism by which GF4 induces apoptosis in human lymphoma JK cells may be related to mitochondrial dysfunction and regulation of the Bcl-2 protein family, specifically by increasing Bax expression and decreasing Bcl-2 expression. [1] Ginsenoside F4 (GF4) is a dammarane-type triterpenoid saponin (ginsenoside) found in Korean red ginseng (steamed root of ginseng), but not in white ginseng. [2] Among the 11 ginsenosides tested, ginsenoside F4 (GF4) and ginsenoside Rg3 showed the most significant inhibitory activity against the expression of MMP-13 in IL-1β-induced SW1353 chondrocytes. [2] This study shows that the mechanism by which ginsenoside F4 (GF4) downregulates MMP-13 expression involves the inhibition of the p38 MAPK signaling pathway. [2] The results showed that ginsenoside F4 (GF4) has therapeutic potential and can be used to prevent the breakdown of cartilage collagen matrix in diseases such as osteoarthritis. [2] The total extract of Korean red ginseng did not show a significant inhibitory effect on MMP-13 expression or GAG release in the test model, which may be due to the low content of active saponins (such as F4) in the crude extract. [2]

C42H70O12

766.9980

766.486

181225-33-2

131751194

White to off-white solid powder

1.3±0.1 g/cm3

851.6±65.0 °C at 760 mmHg

177 - 181 °C

468.9±34.3 °C

0.0±0.6 mmHg at 25°C

1.592

8.32

8

12

8

54

1400

0

CC1C(C(C(C(O1)OC2C(C(C(OC2OC3CC4(C(CC(C5C4(CCC5/C(=C/CC=C(C)C)/C)C)O)C6(C3C(C(CC6)O)(C)C)C)C)CO)O)O)O)O)O

QOMBXPYXWGTFNR-CIAFOILYSA-N

InChI=1S/C42H70O12/c1-20(2)11-10-12-21(3)23-13-16-41(8)29(23)24(44)17-27-40(7)15-14-28(45)39(5,6)36(40)25(18-42(27,41)9)52-38-35(33(49)31(47)26(19-43)53-38)54-37-34(50)32(48)30(46)22(4)51-37/h11-12,22-38,43-50H,10,13-19H2,1-9H3/b21-12+

2-[2-[[3,12-dihydroxy-4,4,8,10,14-pentamethyl-17-[(2E)-6-methylhepta-2,5-dien-2-yl]-2,3,5,6,7,9,11,12,13,15,16,17-dodecahydro-1H-cyclopenta[a]phenanthren-6-yl]oxy]-4,5-dihydroxy-6-(hydroxymethyl)oxan-3-yl]oxy-6-methyloxane-3,4,5-triol

2934.99.9001

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.

Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)

May dissolve in DMSO (in most cases), if not, try other solvents such as H2O, Ethanol, or DMF with a minute amount of products to avoid loss of samples

Note: Listed below are some common formulations that may be used to formulate products with low water solubility (e.g. < 1 mg/mL), you may test these formulations using a minute amount of products to avoid loss of samples.

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Injection Formulation 1: DMSO : Tween 80： Saline = 10 : 5 : 85 (i.e. 100 μL DMSO stock solution → 50 μL Tween 80 → 850 μL Saline)
*Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH ₂ O to obtain a clear solution.
Injection Formulation 2: DMSO : PEG300 ：Tween 80 : Saline = 10 : 40 : 5 : 45 (i.e. 100 μL DMSO → 400 μLPEG300 → 50 μL Tween 80 → 450 μL Saline)
Injection Formulation 3: DMSO : Corn oil = 10 : 90 (i.e. 100 μL DMSO → 900 μL Corn oil)
Example: Take the Injection Formulation 3 (DMSO : Corn oil = 10 : 90) as an example, if 1 mL of 2.5 mg/mL working solution is to be prepared, you can take 100 μL 25 mg/mL DMSO stock solution and add to 900 μL corn oil, mix well to obtain a clear or suspension solution (2.5 mg/mL, ready for use in animals).

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Injection Formulation 4: DMSO : 20% SBE-β-CD in saline = 10 : 90 [i.e. 100 μL DMSO → 900 μL (20% SBE-β-CD in saline)]
*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.
Injection Formulation 5: 2-Hydroxypropyl-β-cyclodextrin : Saline = 50 : 50 (i.e. 500 μL 2-Hydroxypropyl-β-cyclodextrin → 500 μL Saline)
Injection Formulation 6: DMSO : PEG300 : castor oil : Saline = 5 : 10 : 20 : 65 (i.e. 50 μL DMSO → 100 μLPEG300 → 200 μL castor oil → 650 μL Saline)
Injection Formulation 7: Ethanol : Cremophor : Saline = 10： 10 : 80 (i.e. 100 μL Ethanol → 100 μL Cremophor → 800 μL Saline)
Injection Formulation 8: Dissolve in Cremophor/Ethanol (50 : 50), then diluted by Saline
Injection Formulation 9: EtOH : Corn oil = 10 : 90 (i.e. 100 μL EtOH → 900 μL Corn oil)
Injection Formulation 10: EtOH : PEG300：Tween 80 : Saline = 10 : 40 : 5 : 45 (i.e. 100 μL EtOH → 400 μLPEG300 → 50 μL Tween 80 → 450 μL Saline)

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Oral Formulation 1: Suspend in 0.5% CMC Na (carboxymethylcellulose sodium)
Oral Formulation 2: Suspend in 0.5% Carboxymethyl cellulose
Example: Take the Oral Formulation 1 (Suspend in 0.5% CMC Na) as an example, if 100 mL of 2.5 mg/mL working solution is to be prepared, you can first prepare 0.5% CMC Na solution by measuring 0.5 g CMC Na and dissolve it in 100 mL ddH2O to obtain a clear solution; then add 250 mg of the product to 100 mL 0.5% CMC Na solution, to make the suspension solution (2.5 mg/mL, ready for use in animals).

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Oral Formulation 3: Dissolved in PEG400
Oral Formulation 4: Suspend in 0.2% Carboxymethyl cellulose
Oral Formulation 5: Dissolve in 0.25% Tween 80 and 0.5% Carboxymethyl cellulose
Oral Formulation 6: Mixing with food powders

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Note: Please be aware that the above formulations are for reference only. InvivoChem strongly recommends customers to read literature methods/protocols carefully before determining which formulation you should use for in vivo studies, as different compounds have different solubility properties and have to be formulated differently.

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 (Please use freshly prepared in vivo formulations for optimal results.)