| Size | Price | Stock | Qty |
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| 5mg |
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| 10mg |
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| 25mg |
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| 50mg |
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| 100mg |
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| Other Sizes |
| Targets |
TNF-α (tumor necrosis factor-alpha) [1].
Caspase-8, Caspase-3 [1]. BID, BAK, BCL-XL (modulation of expression) [1]. p21 (activation), Vimentin (down-regulation) [2]. |
|---|---|
| ln Vitro |
Hydroxygenkwanin (7-O-methylluteolin) inhibits the growth of C6 glioma cells in a dose-dependent manner [1]. Flow cytometry indicates that hydrogen kwanin decreases the ability to form colonies and mote cells and causes cell cycle arrest. Hydroxygenkwanin causes cell cycle arrest and starts the intrinsic apoptotic pathway by activating p21 [2].
HGK (25 μM) inhibited C6 glioma cell proliferation in a time-dependent manner, reaching maximum anti-glioma effect at 24 h [1]. The IC50 of HGK on C6 glioma cells was 66.12 ± 5.26 μM [1]. At 25 μM for 24 h, HGK induced apoptosis in C6 glioma cells, with 38.2 ± 6.0% of cells showing condensed nuclei by DAPI staining [1]. HGK caused mitochondrial membrane potential (MMP) loss (R/G ratio 1.31 ± 0.11 vs control 7.34 ± 1.42, p<0.01) and mitochondrial swelling with cristae disappearance observed by TEM [1]. HGK induced DNA damage in C6 glioma cells: tail DNA% = 31.01 ± 5.44%, tail moment = 19.22 ± 4.67 (p<0.01 vs control) [1]. HGK (25 μM, 24 h) caused S phase cell cycle arrest in C6 glioma cells (37.24 ± 1.56% vs control 25.67 ± 2.06%, p<0.01) [1]. HGK increased TNF-α level in a concentration-dependent manner from 12.5 μM to 25 μM (p<0.05) [1]. HGK up-regulated BID and BAK protein expression, and down-regulated BCL-XL protein expression in C6 glioma cells [1]. HGK increased caspase-3 and caspase-8 activities in C6 glioma cells (p<0.01 vs control) [1]. In oral squamous cell carcinoma (OSCC) cells, HGK inhibited cell growth dose-dependently in SAS and OECM1 cells after 24 h treatment [2]. HGK (50 μM, 24 h) induced differential gene expression affecting cellular movement, cell cycle, and cellular growth and proliferation in OSCC cells [2]. HGK dose-dependently increased the percentage of sub-G0/G1 phase in SAS and OECM1 cells, and reduced G2/M phase in SAS cells [2]. HGK (25-50 μM) significantly reduced cell migration (wound healing assay) and invasion (transwell assay) in SAS and OECM1 cells [2]. HGK up-regulated p21 in SAS cells but down-regulated p21 in OECM1 cells; increased cleaved PARP, cleaved caspase 9, and H2AX phosphorylation; and decreased vimentin expression [2]. |
| Enzyme Assay |
Hydroxygenkwanin's effect on caspase-3 and caspase-8 activities was measured using colorimetric assay kits. Treated C6 glioma cells were lysed and the supernatants were incubated with specific substrates. The optical density (OD) at 405 nm was measured using a micro-plate reader, and enzyme activities were expressed as percentage relative to the control group [1].
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| Cell Assay |
Cell viability was tested by MTT assay. C6 glioma cells were seeded in 96-well plates at 2×10⁴ cells/well, incubated for 24 h, then treated with HGK (12.5, 25, 50 μM) for 12, 24, and 36 h. OD was measured at 570 nm and inhibition ratio calculated [1].
Apoptosis was assessed by AO/EB staining. Cells were stained with a mixture of acridine orange and ethidium bromide (1 μg/ml each), then observed under fluorescence microscope. Cells were classified as normal, necrotic, early apoptotic, or late apoptotic [1]. Nuclear condensation was evaluated by DAPI staining. Cells were stained with DAPI solution (1 μg/ml) for 10 min at 37°C in the dark, then observed under fluorescence microscope [1]. Mitochondrial membrane potential was measured using JC-1 fluorescent probe. Cells were incubated with JC-1 working solution for 20 min at 37°C in darkness, then photographed using laser scanning confocal microscope [1]. DNA damage was assessed by alkaline comet assay. Cells were collected, suspended in cold PBS, mixed with agarose, and subjected to lysis and electrophoresis. Tail DNA% and tail moment were analyzed using Comet Assay Software [1]. Cell cycle distribution was determined by flow cytometry. Cells were fixed in 70% ethanol, stained with propidium iodide, and analyzed on a flow cytometer [1]. TNF-α level in cell supernatants was measured using radioimmunoassay kit [1]. Western blotting: Total protein was extracted using RIPA lysis buffer, quantified by BCA assay, separated by SDS-PAGE, transferred to PVDF membrane, probed with specific primary antibodies (anti-Bcl-2, anti-Bcl-XL, anti-Bak, anti-Bid, anti-Bax, anti-GAPDH), then HRP-conjugated secondary antibodies, and detected by ECL [1]. For OSCC cells, SAS and OECM1 cells were treated with HGK (25, 50, 75 μM) for 24 h. MTT assay, colony formation assay, wound healing migration assay, transwell invasion assay, and flow cytometry for cell cycle were performed. Western blot used antibodies against PARP, caspase 9, phosphor-H2A.X, p21, E-cadherin, vimentin, and β-actin [2]. |
| Toxicity/Toxicokinetics |
HGK showed low toxicity on normal PC12 cells (a neuron cell line). The IC50 of HGK on PC12 cells was approximately 125.30 ± 12.27 μM, which is far beyond its IC50 on C6 glioma cells (66.12 ± 5.26 μM), indicating low neurotoxicity at low concentrations [1].
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| References | |
| Additional Infomation |
Luteolin 7-methyl ether belongs to the flavonoid class of compounds and is an ether compound. It is the conjugate acid of luteolin-5-ol ester 7-methyl ether. It has been reported that 7-O-methyl luteolin is found in daphne, sage, and other organisms with relevant data.
HGK exerts anti-glioma activity through multiple mechanisms: DNA damage, S phase cell cycle arrest, mitochondrial apoptosis pathway (MMP loss, BID/BAK up-regulation, BCL-XL down-regulation), and TNF-α induced caspase-8/caspase-3 activation [1]. When combined with Apigenin (AP), HGK's anti-glioma effect is synergistically enhanced. AP acts as a sensitizer, and the combination (12.5 μM + 12.5 μM for 24 h) achieved 60.9% inhibition on C6 glioma cells, surpassing BCNU at 25 μM [1]. In oral cancer, HGK induces apoptosis via intrinsic pathway (cleaved caspase 9, cleaved PARP, H2AX phosphorylation), causes cell cycle arrest (p21 activation in SAS cells), and inhibits migration/invasion through vimentin down-regulation [2]. RNA sequencing data for HGK-treated OSCC cells is available in NCBI SRA database (Bioproject: PRJNA559691) [2]. |
| Molecular Formula |
C16H12O6
|
|---|---|
| Molecular Weight |
300.2629
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| Exact Mass |
300.063
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| Elemental Analysis |
C, 64.00; H, 4.03; O, 31.97
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| CAS # |
20243-59-8
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| PubChem CID |
5318214
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| Appearance |
Light yellow to green yellow solid powder
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| Density |
1.5±0.1 g/cm3
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| Boiling Point |
602.7±55.0 °C at 760 mmHg
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| Melting Point |
225-227ºC
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| Flash Point |
230.6±25.0 °C
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| Vapour Pressure |
0.0±1.8 mmHg at 25°C
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| Index of Refraction |
1.697
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| LogP |
2.65
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| Hydrogen Bond Donor Count |
3
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| Hydrogen Bond Acceptor Count |
6
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| Rotatable Bond Count |
2
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| Heavy Atom Count |
22
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| Complexity |
462
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| Defined Atom Stereocenter Count |
0
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| SMILES |
O1C(=C([H])C(C2=C(C([H])=C(C([H])=C12)OC([H])([H])[H])O[H])=O)C1C([H])=C([H])C(=C(C=1[H])O[H])O[H]
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| InChi Key |
RRRSSAVLTCVNIQ-UHFFFAOYSA-N
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| InChi Code |
InChI=1S/C16H12O6/c1-21-9-5-12(19)16-13(20)7-14(22-15(16)6-9)8-2-3-10(17)11(18)4-8/h2-7,17-19H,1H3
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| Chemical Name |
2-(3,4-dihydroxyphenyl)-5-hydroxy-7-methoxychromen-4-one
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| Synonyms |
HGK; 3'Hydroxygenkwanin; 3' Hydroxygenkwanin; 3'-Hydroxygenkwanin; Luteolin 7-methyl ether; Luteolin 7 methyl ether; 7-O-Methylluteolin; 7OMethylluteolin; Luteolin 7methyl ether; 7 O Methylluteolin
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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 : ~10 mg/mL (~33.30 mM)
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|---|---|
| Solubility (In Vivo) |
Solubility in Formulation 1: 0.77 mg/mL (2.56 mM) in 10% DMSO + 90% (20% SBE-β-CD in Saline) (add these co-solvents sequentially from left to right, and one by one), suspension solution; with sonication.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 7.7 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. (Please use freshly prepared in vivo formulations for optimal results.) |
| Preparing Stock Solutions | 1 mg | 5 mg | 10 mg | |
| 1 mM | 3.3304 mL | 16.6522 mL | 33.3045 mL | |
| 5 mM | 0.6661 mL | 3.3304 mL | 6.6609 mL | |
| 10 mM | 0.3330 mL | 1.6652 mL | 3.3304 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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