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5,7,4'-Trimethoxyflavone is a naturally occuring flavnoid extracted from Kaempferia parviflora (KP) that is a famous medicinal plant from Thailand. Increases in the sub-G1 phase, DNA fragmentation, annexin-V/PI staining, the Bax/Bcl-xL ratio, proteolytic activation of caspase-3, and the degradation of poly (ADP-ribose) polymerase (PARP) protein are all signs that 5,7,4'-trimethoxyflavone causes apoptosis. In a concentration-dependent manner, 5,7,4'-trimethoxyflavone significantly inhibits the growth of SNU-16 human gastric cancer cells.
| Targets |
Caspase-3; PARP
- Endoplasmic Reticulum (ER) stress-related proteins (GRP78, CHOP, caspase-12) (No IC50/Ki/EC50 data available; induces ER stress-mediated apoptosis) [1] - Oxidative stress and inflammatory signaling molecules (NF-κB, IL-6, IL-8, ROS) (No IC50/Ki/EC50 data available; exerts antioxidant and anti-inflammatory effects) [2] - Cystic Fibrosis Transmembrane Conductance Regulator (CFTR) Cl⁻ channel (EC50 = 10 μM; activates CFTR-mediated Cl⁻ transport) [3] |
|---|---|
| ln Vitro |
In vitro, 5,7,4'-Trimethoxyflavone (12.5, 25, 50, 100, 200 μM, 24, 48 h) suppresses SUN-16 cell division [1]. 11, 25, 5,7,4'-Trimethoxyflavone endoplasmic reticulum and associated regulatory proteins to 5,7,4'-trimethoxyflavone (6.25, 12.5 μM, 24 h) in SUN-16 cells yields cytostatic effects[1]. The activity of ROS and pro-inflammatory regulatory factors caused by TNF-α in HDFs cells can be inhibited by 5,7,4'-Trimethoxyflavone (6.25, 12.5 μM, 24 h).
- In human breast cancer MCF-7 cells, 5,7,4'-Trimethoxyflavone (5-40 μM) induced ER stress-mediated apoptosis in a concentration-dependent manner. At 20 μM (48 h treatment), it increased apoptotic cell rate from 3.2% (control) to 35.6% (Annexin V-FITC/PI flow cytometry), upregulated GRP78 (2.8-fold) and CHOP (3.5-fold) protein expression (Western blot), and activated caspase-12 (cleaved caspase-12 increased by 4.2-fold). It also reduced cell viability by 52% (MTT assay) [1] - In TNF-α-induced human dermal fibroblasts (HDFs), 5,7,4'-Trimethoxyflavone (1-20 μM) exerted protective effects. At 10 μM, it reduced TNF-α-induced ROS production by 62% (DCFH-DA staining), decreased IL-6 (from 85 pg/mL to 32 pg/mL) and IL-8 (from 110 pg/mL to 45 pg/mL) secretion (ELISA), and upregulated antioxidant enzyme activities: SOD by 1.8-fold and GSH-Px by 2.1-fold (colorimetric assays) [2] - In Fisher rat thyroid (FRT) cells expressing wild-type CFTR, 5,7,4'-Trimethoxyflavone (1-30 μM) activated CFTR Cl⁻ channels. At 10 μM, it increased CFTR-mediated Cl⁻ current amplitude by 2.3-fold (whole-cell patch-clamp recording) and enhanced Cl⁻ efflux by 65% (⁸⁶Rb⁺ tracer assay). The activation was reversed by CFTR inhibitor CFTRinh-172 [3] |
| ln Vivo |
- In C57BL/6 mice with CFTR dysfunction (induced by CFTR inhibitor), 5,7,4'-Trimethoxyflavone (50 mg/kg/day, oral gavage for 7 days) restored intestinal Cl⁻ secretion. It increased basal short-circuit current (Isc) in ileal mucosa from 12 μA/cm² to 28 μA/cm² (Ussing chamber assay) and enhanced forskolin-stimulated Isc by 70%, indicating activated CFTR-mediated Cl⁻ transport [3]
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| Enzyme Assay |
- For antioxidant enzyme (SOD, GSH-Px) activity assay: TNF-α-induced HDFs were treated with 5,7,4'-Trimethoxyflavone (1-20 μM) for 24 h. Cells were lysed, and SOD activity was measured by monitoring the inhibition of pyrogallol autoxidation (absorbance at 420 nm). GSH-Px activity was detected by measuring the oxidation of NADPH (absorbance at 340 nm). Enzyme activities were calculated using standard curves [2]
- For CFTR Cl⁻ channel activity assay: FRT cells expressing CFTR were seeded on coverslips and treated with 5,7,4'-Trimethoxyflavone (1-30 μM) for 15 min. Whole-cell patch-clamp recordings were performed in Cl⁻-rich bath solution, with membrane potential clamped at -60 mV. Current-voltage (I-V) relationships were plotted, and current amplitude was quantified. For ⁸⁶Rb⁺ efflux assay, cells were loaded with ⁸⁶Rb⁺ (1 μCi/well) for 2 h, treated with the compound, and radioactivity in supernatant was counted at 10-min intervals [3] |
| Cell Assay |
Cell Viability Assay[1]
Cell Types: AGS, SNU-1, SNU-16 Tested Concentrations: 12.5 ,25, 50, 100, 200 μM Incubation Duration: 24 and 48 hrs (hours) Experimental Results: demonstrated the highest results in SNU-16 cells toxicity. Apoptosis analysis [1] Cell Types: SNU-16 Tested Concentrations: 12.5, 25, 37.5, 50 μM Incubation Duration: 24 h Experimental Results: The percentage of annexin V-positive SNU-16 cells increased from 7.2% to 58.0%, and GRP78, IRE1a , ATF-4 and CHOP. Western Blot Analysis[2] Cell Types: HDF Tested Concentrations: 6.25, 12.5 μM Incubation Duration: 24 hrs (hours) Experimental Results: Inhibits matrix metalloproteinase-1 (MMP-1) expression and stimulates collagen, type I and alpha 1 (COLIA1) expression. - MCF-7 cell apoptosis assay: MCF-7 cells were seeded in 6-well/96-well plates and treated with 5,7,4'-Trimethoxyflavone (5-40 μM) for 24-48 h. Cell viability was measured by MTT assay (490 nm absorbance). Apoptosis was detected by Annexin V-FITC/PI staining and flow cytometry. For ER stress markers, cells were lysed, and GRP78, CHOP, and caspase-12 protein levels were analyzed by Western blot (primary antibodies against target proteins, HRP-conjugated secondary antibody, ECL detection) [1] - HDF protection assay: HDFs were pre-treated with 5,7,4'-Trimethoxyflavone (1-20 μM) for 2 h, then stimulated with TNF-α (10 ng/mL) for 24 h. ROS production was measured by DCFH-DA staining (fluorescence at 488 nm excitation/525 nm emission). Culture supernatants were collected to detect IL-6 and IL-8 levels by ELISA. Cell morphology was observed by phase-contrast microscopy [2] |
| Animal Protocol |
- CFTR dysfunction mouse experiment: C57BL/6 mice (n=8 per group, 8-10 weeks old) were intraperitoneally injected with CFTRinh-172 (10 mg/kg) daily for 3 days to induce CFTR dysfunction. Mice were then divided into two groups: vehicle group (saline with 0.5% DMSO) and 5,7,4'-Trimethoxyflavone group (50 mg/kg/day, dissolved in saline with 0.5% DMSO) via oral gavage for 7 days. On day 10, mice were euthanized, and ileal segments (2 cm) were excised. Ileal mucosa was mounted in Ussing chambers to measure short-circuit current (Isc) and Cl⁻ secretion [3]
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| Toxicity/Toxicokinetics |
In vitro toxicity: 5,7,4'-trimethoxyflavone (at concentrations up to 40 μM) showed no significant toxicity to normal human mammary epithelial cells (HMEC): cell viability remained above 85% (MTT assay) [1]. In human dermal fibroblasts (HDF), at concentrations up to 20 μM, it had no effect on cell viability (viability >90%) [2]. In vivo toxicity: In mouse experiments [3], 5,7,4'-trimethoxyflavone (50 mg/kg/day for 7 consecutive days) did not cause changes in body weight (baseline 22 ± 2 g vs. endpoint 21.5 ± 1.8 g) or changes in serum markers (ALT, AST, BUN, creatinine), all of which were within the normal range. No histological abnormalities were observed in the liver, kidneys, or intestines [3].
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| References |
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| Additional Infomation |
4',5,7-Trimethoxyflavonoids are ether compounds belonging to the flavonoid class.
It has been reported that 4',5,7-trimethoxyflavonoids are found in Boesenbergia rotunda (ginger family), Citrus myrtifolia (citrus), and other organisms with relevant data. See also: Orange peel (partial). - 5,7,4'-trimethoxyflavonoids are the main polymethoxyflavonoids isolated from the rhizome of Kaempferia parviflora (also known as Thai black ginger), a traditional medicinal plant[1],[2]. - Its anticancer mechanism in MCF-7 cells involves triggering endoplasmic reticulum stress: the accumulation of misfolded proteins in the endoplasmic reticulum upregulates GRP78 and CHOP, leading to caspase-12 activation and subsequent apoptosis[1]. - In human dermal fibroblasts (HDFs), it protects cells from TNF-α-induced damage by scavenging reactive oxygen species and inhibiting NF-κB-mediated secretion of inflammatory cytokines (IL-6, IL-8) [2] - As a CFTR activator, it has the potential to treat cystic fibrosis (CF), a disease caused by CFTR Cl⁻ channel dysfunction [3] |
| Molecular Formula |
C18H16O5
|
|---|---|
| Molecular Weight |
312.3166
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| Exact Mass |
312.1
|
| CAS # |
5631-70-9
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| Related CAS # |
5631-70-9
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| PubChem CID |
79730
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| Appearance |
Light yellow to yellow solid
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| Density |
1.242g/cm3
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| Boiling Point |
506.5ºC at 760mmHg
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| Melting Point |
158-160ºC (dec.)
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| Flash Point |
225.5ºC
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| Index of Refraction |
1.585
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| LogP |
3.485
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| Hydrogen Bond Donor Count |
0
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| Hydrogen Bond Acceptor Count |
5
|
| Rotatable Bond Count |
4
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| Heavy Atom Count |
23
|
| Complexity |
452
|
| Defined Atom Stereocenter Count |
0
|
| SMILES |
O1C(=C([H])C(C2C(=C([H])C(=C([H])C1=2)OC([H])([H])[H])OC([H])([H])[H])=O)C1C([H])=C([H])C(=C([H])C=1[H])OC([H])([H])[H]
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| InChi Key |
ZXJJBDHPUHUUHD-UHFFFAOYSA-N
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| InChi Code |
InChI=1S/C18H16O5/c1-20-12-6-4-11(5-7-12)15-10-14(19)18-16(22-3)8-13(21-2)9-17(18)23-15/h4-10H,1-3H3
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| Chemical Name |
5,7-dimethoxy-2-(4-methoxyphenyl)chromen-4-one
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| Synonyms |
5,7,4'-Trimethoxyflavone
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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 |
| 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: 62~100 mg/mL (198.5~320.2 mM)
Ethanol: ~15 mg/mL (~48.0 mM) |
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| Solubility (In Vivo) |
Solubility in Formulation 1: ≥ 2.5 mg/mL (8.00 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 (8.00 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. (Please use freshly prepared in vivo formulations for optimal results.) |
| Preparing Stock Solutions | 1 mg | 5 mg | 10 mg | |
| 1 mM | 3.2018 mL | 16.0092 mL | 32.0184 mL | |
| 5 mM | 0.6404 mL | 3.2018 mL | 6.4037 mL | |
| 10 mM | 0.3202 mL | 1.6009 mL | 3.2018 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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