Art. -Nr.: HY-W097625

6-Methoxyflavone

Kundenbewertung

Based on 1 Customer Validation

6-Methoxyflavone is an orally active methoxyflavone. 6-Methoxyflavone suppresses neuroinflammation in microglia through the inhibition of TLR4/MyD88/p38 MAPK/NF-κB dependent pathways and the activation of HO-1/NQO-1 signaling. 6-Methoxyflavone induces S-phase arrest through the CCNA2/CDK2/p21CIP1 signaling pathway in HeLa cells. 6-Methoxyflavone inhibits NFAT Translocation into the nucleus and suppresses T cell activation. 6-Methoxyflavone partially restores chronic ethanol-induced behavioral deficits in mice. 6-Methoxyflavone antagonizes chronic constriction injury and diabetes associated neuropathic nociception expression. 6-Methoxyflavone can be used for the study of cancer, inflammation and neurological diseases.

Nur für Forschungszwecke. Wir verkaufen nicht an Patienten.

Reinheit: 99.73%
CAS. Nr.: 26964-24-9
Formel: C₁₆H₁₂O₃
Molecular Weight:252.27

Speicherung:

Powder -20°C, 3 years , 4°C, 2 years ; In solvent -80°C, 6 months , -20°C, 1 month

6-Methoxyflavone Chemical Structure

CAS. Nr.: 26964-24-9

Größe

Preis

Verfügbarkeit

Menge

Amount: USD 0.00

* Bitte wählen Sie Menge, bevor Sie Artikel hinzufügen.

Top Publications Citing

Use of MCE Products

Fluorescent Dye

Strong Fluorescence Signal / Multi-Disciplinary Applications / High Fluorescence Specificity

Biologische Aktivität
- Beschreibung
- Cellular Effect
- In Vitro
- In Vivo
Chemical Information
Lösungsmittel & Löslichkeit
- In Vitro
Reinheit & Dokumentation
Verweise
Help & FAQs
Classifications
Bioz

Biologische Aktivität

Beschreibung

Alle Toll-like Receptor (TLR) Isoform-spezifische Produkte anzeigen :

Alle NF-κB Isoform-spezifische Produkte anzeigen :

Alle p38 MAPK Isoform-spezifische Produkte anzeigen :

Alle Heme Oxygenase (HO) Isoform-spezifische Produkte anzeigen :

HO-1
HO-2

Cellular Effect

Cell Line	Type	Value	Description	References
A2780 ADR	IC₅₀	13 μM Compound: 8	Inhibition of P-gp expressed in A2780adr cells by calcein AM accumulation assay Inhibition of P-gp expressed in A2780adr cells by calcein AM accumulation assay	[PMID: 21354800]
MCF7	IC₅₀	10 μM Compound: 8	Inhibition of BCRP expressed in MCF-7 MX cells using Hoechst 33342 staining Inhibition of BCRP expressed in MCF-7 MX cells using Hoechst 33342 staining	[PMID: 21354800]
MDCK	IC₅₀	15 μM Compound: 8	Inhibition of MDR1 expressed in MDCK cells using rhodamine 123 staining by flow cytometry Inhibition of MDR1 expressed in MDCK cells using rhodamine 123 staining by flow cytometry	[PMID: 21354800]
MDCK	IC₅₀	3.4 μM Compound: 8	Inhibition of BCRP expressed in MDCK cells using Hoechst 33342 staining Inhibition of BCRP expressed in MDCK cells using Hoechst 33342 staining	[PMID: 21354800]

In Vitro

6-Methoxyflavone (20-160 μM, 24-72 h) inhibits proliferation of HaCaT, HeLa, C33A, and SiHa cells, with HeLa cells being most sensitive (IC₅₀: 94.05 μM at 24 h, 62.24 μM at 48 h, 52.12 μM at 72 h)^[1].
6-Methoxyflavone (20-160 μM, 48 h) induces S-phase arrest in HeLa cells in a concentration-dependent manner^[1].
6-Methoxyflavone (65 μM, 48 h) downregulates mRNA and protein expression of CCNA2 and CDK2, while upregulating CCND1, CCNE1, CDK6, and p21CIP1 in HeLa cells, via the CCNA2/CDK2/p21CIP1 pathway^[1].
6-Methoxyflavone (3-30 μM, pretreatment for 1 h) suppresses LPS-induced phosphorylation of NF-κB p65, IκB and reduces LPS (HY-D1056)-induced expression of TLR4, MyD88 and phosphorylation of p38 MAPK, JNK in BV2 microglia^[1]. 6-Methoxyflavone (3-30 μM, pretreatment for 1 h) suppresses TLR4/MyD88/p38 MAPK/NF-κB dependent pathways and activates HO-1/NQO-1 signaling in LPS-stimulated BV2 microglia^[3].
6-Methoxyflavone (5-20 μM, 1-24 h) inhibits the enhancer activity of CNS-9, reducing IL-10 expression in EL4 T cells and primary Th2 cells^[5].
6-Methoxyflavone (5-20 μM, 1-72 h) inhibits the translocation of NFAT1 into the nucleus in Th2 cells and ex vivo CD4⁺ T cells and inhibits proliferation of CD4⁺ T cells and CD19⁺ B cells isolated from atopic dermatitis mice and reduces IgE production by B cells^[5].

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

Cell Cycle Analysis^[1]

Cell Line:

HeLa cells
Concentration:

20, 40, 80, 120, 160 μM
Incubation Time:

48 h
Result:

Induced S-phase arrest in HeLa cells in a concentration-dependent manner.

Cell Cycle Analysis^[1]

Cell Line:

HeLa cells
Concentration:

65 μM
Incubation Time:

48 h
Result:

Downregulated mRNA expression of CCNA2 and CDK2.
Upregulated CCND1, CCNE1, CDK6, and p21CIP1 in HeLa cells.

ELISA Assay^[3]

Cell Line:

LPS-stimulated BV2 microglia
Concentration:

3, 10, 30 μM
Incubation Time:

Pretreatment for 1 h
Result:

Decreased the levels of pro-inflammatory factors (IL-1β, IL-6, TNF-α, PGE2) in LPS-stimulated BV2 microglia.

Western Blot Analysis^[3]

Cell Line:

LPS-stimulated BV2 microglia
Concentration:

3, 10, 30 μM
Incubation Time:

Pretreatment for 1 h
Result:

Suppressed LPS-induced phosphorylation of NF-κB p65 and IκB.
reduced LPS-induced expression of TLR4, MyD88 and phosphorylation of p38 MAPK, JNK.
Decreased iNOS and COX-2 expression.
Increased HO-1 and NQO1 expression.

In Vivo

6-Methoxyflavone (25-75 mg/kg, p.o., once daily 15 min before ethanol, 24 days) partially restores chronic ethanol-induced behavioral deficits in mice^[2].
6-Methoxyflavone (10-30 μM, pretreatment for 1 h before LPS (100 ng/mL), exposure for 24 h) is non-toxic to zebrafish embryos and inhibits LPS-induced NO generation^[3].
6-Methoxyflavone (25-50 mg/kg, i.p., once daily for 4 days before LPS injection 3 h prior to sacrifice) prevents LPS-induced microgliosis in the prefrontal cortex and substantia nigra in mice^[3].
6-Methoxyflavone (25-75 mg/kg, i.p., once daily for 21 days post-surgery) antagonizes chronic constriction injury (CCI) and Streptozotocin (STZ) (HY-13753)-induced static (pressure) and dynamic (light brushing) hindpaw allodynia, heat/cold and pressure hyperalgesia in rats^[4].
6-Methoxyflavone (20-100 mg/kg, i.g., five times per week for 6 weeks) ameliorates symptoms of experimental atopic dermatitis in BALB/c mice^[5].

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

Animal Model:

Male BALB/c mice (22–28 g) were used, with chronic ethanol-induced cognitive impairment models established by oral administration of 25% w/v ethanol (2.0 g/kg daily) for 24 consecutive days, followed by 6 days of ethanol withdrawal^[2]
Dosage:

25, 50, 75 mg/kg
Administration:

p.o. once daily 15 min before ethanol for 24 days
Result:

Restored locomotor activity suppressed by chronic ethanol and enhanced activity during abstinence and post-withdrawal.
Improved novel object recognition, with increased exploration time on days 12, 24, during abstinence, and post-withdrawal.
Enhanced Morris water maze performance.
Ameliorated Y-maze deficits and enhanced nest-building.
Increased socialization, with all doses raising exploration time with novel juveniles at all stages.
Raised frontal cortical dopamine and vitamin C and reversed frontal cortical noradrenaline reduction.
Increased hippocampal dopamine and elevated hippocampal noradrenaline.

Animal Model:

3-month-old male C57BL/6 mice were used, with LPS-induced brain inflammatory models established by intraperitoneal injection of LPS (5 mg/kg) 3 h before sacrifice, following pretreatment with 6-methoxyflavone or PBS for 4 days^[3]
Dosage:

25, 50 mg/kg
Administration:

i.p. once daily for 4 days before LPS injection 3 h prior to sacrifice
Result:

Reduced microglial cell density in the prefrontal cortex (PFC) and substantia nigra (SN) after LPS stimulation.
Decreased cell size of Iba1-positive microglia in PFC and SN, with 50 mg/kg showing significant effects.
Increased cell process length of microglia in PFC and SN, improving morphological abnormalities induced by LPS.
Suppressed phosphorylation of p38 in PFC and SN, inhibiting overactivation of the p38 MAPK signaling pathway.
Reduced MyD88 protein expression in SN, downregulating the TLR4/MyD88 dependent pathway.

Animal Model:

Sprague-Dawley rats (male, 300-450 g) were used, with CCI-induced mononeuropathy models established by exposing the sciatic nerve and applying four double knot ligatures (1 mm apart) prior to its trifurcation^[4]
Dosage:

25, 50, 75 mg/kg
Administration:

i.p. once daily for 21 days
Result:

Reduced static mechanical allodynia, as evidenced by increased paw withdrawal threshold to von Frey filaments in the operated hindpaw. Alleviated dynamic mechanical allodynia, shown by prolonged paw withdrawal latency to light brushing with a cotton bud. Attenuated heat hyperalgesia.
Diminished cold allodynia.
Relieved pin-prick hyperalgesia.
Improved locomotor activity.
Enhanced motor coordination.
Showed normal gait, reflected by reduced overlap distance between forepaw and hindpaw placement in footprint analysis.

Animal Model:

Sprague-Dawley rats (female, 180-220 g) were used, with STZ-induced diabetic polyneuropathy models established by a single intraperitoneal injection of streptozotocin (50 mg/kg) after 16 h fasting, and rats with random blood glucose levels exceeding 250 mg/dL 72 h post-injection were included in the experiment^[4]
Dosage:

25, 50, 75 mg/kg
Administration:

i.p. once daily for 21 days
Result:

Reduced static mechanical allodynia in bilateral hindpaws.
Alleviated dynamic mechanical allodynia in bilateral hindpaws.
Attenuated heat hyperalgesia in bilateral hindpaws.
Relieved static mechanical vulvodynia.
Alleviated dynamic mechanical vulvodynia.
Improved locomotor activity.
Enhanced motor coordination.
Showed normal gait, shown by reduced overlap distance between forepaw and hindpaw placement in footprint analysis.

Animal Model:

BALB/c mice were used, with experimental atopic dermatitis models established by stripping the ear surface five times with surgical tape, painting with 20 μL 4% 2,4-dinitrochlorobenzene (dissolved in acetone/olive oil solution at a 1:3 ratio) for sensitization, and then challenging the ears with 20 μL 2% dinitrochlorobenzene and 20 μL dust mite extracts (10 mg/mL) dissolved in PBS containing 0.5% Tween 20 once per week for 6 weeks^[5]
Dosage:

20, 100 mg/kg
Administration:

i.g. five times per week for 6 weeks
Result:

Reduced infiltration of lymphocytes in the ears.
Decreased thickness of the epidermis.
Lowered serum IgE levels.
Ameliorated symptoms such as erythema, horny substance, dryness, and scaling.

Chemical Information

CAS. Nr. 26964-24-9
Appearance Solid
Molecular Weight 252.27
Formel C₁₆H₁₂O₃
Color Light yellow to yellow
SMILES

O=C1C=C(C2=CC=CC=C2)OC3=CC=C(OC)C=C13
Structure Classification
- Flavonoids
- Flavones
Initial Source
Versand

Room temperature in continental US; may vary elsewhere.

Speicherung

Powder	-20°C	3 years
	4°C	2 years
In solvent	-80°C	6 months
	-20°C	1 month

Lösungsmittel & Löslichkeit

In Vitro:

DMSO : 5 mg/mL (19.82 mM; ultrasonic and warming and heat to 60°C; Hygroscopic DMSO has a significant impact on the solubility of product, please use newly opened DMSO)

View the Complete Stock Solution Preparation Table

Preparing Stock Solutions

View the Complete Stock Solution Preparation Table

Concentration Solvent Mass

1 mg

5 mg

10 mg

Concentration

Solvent

Mass

1 mM

3.9640 mL

19.8200 mL

39.6401 mL

5 mM

0.7928 mL

3.9640 mL

7.9280 mL

10 mM

0.3964 mL

1.9820 mL

3.9640 mL

Please refer to the solubility information to select the appropriate solvent. Once prepared, please aliquot and store the solution to prevent product inactivation from repeated freeze-thaw cycles.

Storage method and period of stock solution: -80°C, 6 months; -20°C, 1 month. When stored at -80°C, please use it within 6 months. When stored at -20°C, please use it within 1 month.

Molaritätsrechner

Mass (g) = Concentration (mol/L) × Volume (L) × Molecular Weight (g/mol)

Mass Mass

Konzentration Konzentration

Volumen Volumen

Molecular Weight Molecular Weight

Verdünnungsrechner

Konzentration _{(Stammlösung)} × Volumen _{(Stammlösung)} = Konzentration _{(Ziellösung)} × Volumen _{(Ziellösung)}

Konzentration _{(Stammlösung)} Konzentration _{(Stammlösung)}

Volumen _{(Stammlösung)} Volumen _{(Stammlösung)}

Konzentration _{(Ziellösung)} Konzentration _{(Ziellösung)}

Volumen _{(Ziellösung)} Volumen _{(Ziellösung)}

Reinheit & Dokumentation

Select Batch:

Reinheit: 99.98%

Assay: 99.98%

ee.: 99.98%

Data Sheet (290 KB)
SDS (394 KB)
- English - EN (394 KB)
- Français - FR (394 KB)
- Deutsch - DE (394 KB)
- Norwegian - NO (394 KB)
- Español - ES (394 KB)
- Swedish - SV (394 KB)
- Italian - IT (394 KB)
- Korean - KR (394 KB)
- Portuguese - PT (394 KB)
COA (2659 KB)
Elemental Analysis Report (2659 KB)
HNMR (2659 KB)
CNMR (2659 KB)
RP-HPLC (2659 KB)
NP-HPLC (2659 KB)
MS (2659 KB)
LCMS (2659 KB)
IR (2659 KB)
GC (2659 KB)
OR (2659 KB)
SDS-PAGE (2659 KB)
SEC-HPLC (2659 KB)
Other Report (2659 KB)
Handling Instructions (2659 KB)

Verweise

[1]. Zhang C, Quan Y, Yang L, Bai Y, Yang Y. 6-Methoxyflavone induces S-phase arrest through the CCNA2/CDK2/p21CIP1 signaling pathway in HeLa cells. Bioengineered. 2022 Mar;13(3):7277-7292. [Content Brief]

[2]. Arif M, Rauf K, Rehman NU, Tokhi A, Ikram M, Sewell RD. 6-Methoxyflavone and Donepezil Behavioral Plus Neurochemical Correlates in Reversing Chronic Ethanol and Withdrawal Induced Cognitive Impairment. Drug Des Devel Ther. 2022 May 28;16:1573-1593. [Content Brief]

[3]. Chen WF, et al. 6-methoxyflavone suppresses neuroinflammation in lipopolysaccharide- stimulated microglia through the inhibition of TLR4/MyD88/p38 MAPK/NF-κB dependent pathways and the activation of HO-1/NQO-1 signaling. Phytomedicine. 2022 May;99:154025. [Content Brief]

[4]. Shahid M, et al. 6-Methoxyflavone antagonizes chronic constriction injury and diabetes associated neuropathic nociception expression. Biochem Biophys Res Commun. 2024 Sep 10;724:150217. [Content Brief]

[5]. So JS, et al. 6-Methoxyflavone inhibits NFAT translocation into the nucleus and suppresses T cell activation. J Immunol. 2014 Sep 15;193(6):2772-83. [Content Brief]

Help & FAQs

How should lyophilized recombinant proteins be reconstituted and stored?

1. Before opening the cap, centrifuge the vial at 13000 rpm for 20-30 seconds. This step will ensure that any lyophilized powder that may have adhered to the cap or walls is collected at the bottom of the vial, minimizing the risk of product loss.

Complete Stock Solution Preparation Table

Storage method and period of stock solution: -80°C, 6 months; -20°C, 1 month. When stored at -80°C, please use it within 6 months. When stored at -20°C, please use it within 1 month.

Optional Solvent	Concentration Solvent Mass	1 mg	5 mg	10 mg	25 mg
DMSO	1 mM	3.9640 mL	19.8200 mL	39.6401 mL	99.1002 mL
	5 mM	0.7928 mL	3.9640 mL	7.9280 mL	19.8200 mL
	10 mM	0.3964 mL	1.9820 mL	3.9640 mL	9.9100 mL
	15 mM	0.2643 mL	1.3213 mL	2.6427 mL	6.6067 mL

Keywords

Produktname:
Art. -Nr.:
Menge:
MCE Japan Authorized Agent:

Produktname:
CAS. Nr.:
Species:
Reinheit:
Menge:

6-Methoxyflavone

Cell Cycle/DNA Damage Compound Library

Immunology/Inflammation Compound Library

Kinase Inhibitor Library

MAPK Compound Library

Metabolism/Protease Compound Library

NF-κB Signaling Compound Library

Stem Cell Signaling Compound Library

Natural Product Library

Anti-Cancer Compound Library

Small Molecule Immuno-Oncology Compound Library

Anti-Aging Compound Library

Antioxidant Compound Library

Differentiation Inducing Compound Library

Reprogramming Compound Library

Anti-diabetic Compound Library

Oxygen Sensing Compound Library

Endoplasmic Reticulum Stress Compound Library

Medicine Food Homology Compound Library

Glycolysis Compound Library

Pyroptosis Compound Library

Orally Active Compound Library

Traditional Chinese Medicine Active Compound Library

Flavonoids Library

Anti-Breast Cancer Compound Library

Anti-Lung Cancer Compound Library

Anti-Pancreatic Cancer Compound Library

Anti-Blood Cancer Compound Library

Anti-Cancer Metabolism Compound Library

Neurodegenerative Disease-related Compound Library

Anti-Obesity Compound Library

Angiogenesis-Related Compound Library

Transcription Factor-Targeted Library

Anti-Liver Cancer Compound Library

Anti-Cancer Natural Product Library

Antidepressant Compound Library

Anti-inflammatory Traditional Chinese Medicine Active Compound Library

Plant-Sourced Natural Product Library

Anti-Prostate Cancer Compound Library

Anti-Pulmonary Fibrosis Compound Library

Osteogenesis Compound Library

Cancer Stem Cells Compound Library

Pain-Related Compound Library

Membrane Protein-targeted Compound Library

Membrane Receptor-targeted Compound Library

Autoimmune Disease Compound Library

Serine/Threonine Kinase Inhibitor Library

Allosteric Modulators (AMs) Compound Library

Anti-Hematopathy Compound Library

Anti-Ovarian Cancer Compound Library

Multi-Target Compound Library

Radioprotector Library

Bioactive Compound Library Max

MCE Bioactive Compound Library

Natural Product Library Plus

Natural Product and Natural Product-Like Compound Library

Bioactive Compound Library

Anti-Gastric Cancer Compound Library

Anti-Fibrosis Compound Library

Protein Kinase Compound Library

Non-Alcoholic Fatty Liver Disease (NAFLD) Compound Library

RO5 Drug-like Natural Product Library

Cell Proliferation Compound Library

High-Throughput Bioactive Compound Library

High-Throughput Natural Product Library

Anti-Rheumatic Arthritis Compound Library

Diarrhea-Related Traditional Chinese Medicine Active Compound Library

Pattern Recognition Receptors Library

Mongolian Medicine Compound Library

Lactylation Compound Library

Mass Spectrometry Natural Product Library

Alle Toll-like Receptor (TLR) Isoform-spezifische Produkte anzeigen

Alle NF-κB Isoform-spezifische Produkte anzeigen

Alle p38 MAPK Isoform-spezifische Produkte anzeigen

Alle Heme Oxygenase (HO) Isoform-spezifische Produkte anzeigen

Biologische Aktivität

Chemical Information

Lösungsmittel & Löslichkeit

Reinheit & Dokumentation

Verweise