2. Apoptosis Autophagy PI3K/Akt/mTOR MAPK/ERK Pathway Cell Cycle/DNA Damage Metabolic Enzyme/Protease Stem Cell/Wnt TGF-beta/Smad JAK/STAT Signaling NF-κB Immunology/Inflammation
  3. Apoptosis Autophagy PI3K JNK mTOR p38 MAPK CDK MMP TGF-beta/Smad STAT β-catenin Reactive Oxygen Species (ROS) Bcl-2 Family Caspase
  4. Sotetsuflavone

Sotetsuflavone is a flavonoid that can be isolated from Cycas revolute. Sotetsuflavone inhibits phosphorylation of PI3K, Akt, mTOR, JNK, and p38 MAPK; modulates expression of Cyclin D1, CDK4, Bcl-2, Bax, cleaved caspases 3/9, MMP-9, TGF-β, STAT3, and β-catenin. Sotetsuflavone induces G0/G1 cell cycle arrest, apoptosis, autophagy, and intracellular ROS elevation, inhibits cancer cell proliferation. Sotetsuflavone inhibits tumor growth in mouse tumor xenograft models. Sotetsuflavone can be used for the research of non-small cell lung cancer and Crohn’s disease.

For research use only. We do not sell to patients.

Sotetsuflavone

Sotetsuflavone Chemical Structure

CAS No. : 2608-21-1

Size Stock
50 mg   Get quote  
100 mg   Get quote  
250 mg   Get quote  

* Please select Quantity before adding items.

This product is a controlled substance and not for sale in your territory.

Sotetsuflavone Related Antibodies

Top Publications Citing Use of Products

View All PI3K Isoform Specific Products:

View All Isoforms
PI3Kα PI3Kβ PI3Kγ PI3Kδ PI3KC2α PI3KC2β PI3KC2γ Vps34 PI3K PI3KC3 p120γ

View All JNK Isoform Specific Products:

View All Isoforms
JNK1 JNK2 JNK3 JNK

View All mTOR Isoform Specific Products:

View All Isoforms
mTOR mTORC1 mTORC2

View All p38 MAPK Isoform Specific Products:

View All Isoforms
p38 MAPK Akt1 p38α p38β MAPK13 p38δ p38γ

View All CDK Isoform Specific Products:

View All Isoforms
CDK1 CDK2 CDK3 CDK4 CDK5 CDK6 CDK7 CDK8 CDK9 CDK11 CDK12 CDK13 CDK14 CDK16 CDK19 CDC CLK Pho85 CDK10 CDK15 CDK17 CDK18 CDK20 PITSLRE

View All MMP Isoform Specific Products:

View All Isoforms
MMP-1 MMP-2 MMP-3 MMP-8 MMP-9 MMP-13 MMP-14 MMP-17 ADAM10 ADAM17 MMP-7 MMP-12 MMP-10 MMP ADAM8 MMP-19

View All STAT Isoform Specific Products:

View All Isoforms
STAT3 STAT5 STAT6 STAT1

View All Bcl-2 Family Isoform Specific Products:

View All Isoforms
Bcl-2 Bcl-xL Bcl-W Mcl-1 Bfl-1 Bcl-B Bax Bak Bim BNIP3 Bad

View All Caspase Isoform Specific Products:

View All Isoforms
Caspase 1 Caspase 2 Caspase 3 Caspase 4 Caspase 5 Caspase 6 Caspase 7 Caspase 8 Caspase 9 Caspase 10 Caspase 12 Caspase Caspase 11 Caspase-13

  • Biological Activity

  • Purity & Documentation

  • References

  • Customer Review

Description

Sotetsuflavone is a flavonoid that can be isolated from Cycas revolute. Sotetsuflavone inhibits phosphorylation of PI3K, Akt, mTOR, JNK, and p38 MAPK; modulates expression of Cyclin D1, CDK4, Bcl-2, Bax, cleaved caspases 3/9, MMP-9, TGF-β, STAT3, and β-catenin. Sotetsuflavone induces G0/G1 cell cycle arrest, apoptosis, autophagy, and intracellular ROS elevation, inhibits cancer cell proliferation. Sotetsuflavone inhibits tumor growth in mouse tumor xenograft models. Sotetsuflavone can be used for the research of non-small cell lung cancer and Crohn’s disease[1][2][3][4][5].

In Vitro

Sotetsuflavone (64-128 μmol/L; 24 h) inhibits the PI3K/Akt/mTOR signaling pathway in A549 and H1650 non-small cell lung cancer cells[1].
Sotetsuflavone (5-200 μmol/L; 24 h) dose-dependently inhibits H1650 cell viability with an IC50 of 67.54 μmol/L[1].
Sotetsuflavone (64-128 μmol/L; 14 days) significantly inhibits colony formation by A549 and H1650 non-small cell lung cancer cells[1].
Sotetsuflavone (64-128 μmol/L; 24 h) significantly inhibits the migration of H1650 cells[1].
Sotetsuflavone (64-128 μmol/L) significantly inhibits the invasion of H1650 non-small cell lung cancer cells[1].
Sotetsuflavone (64-128 μmol/L; 24 h) significantly induces apoptosis in both A549 and H1650 non-small cell lung cancer cells[1].
Sotetsuflavone (64-128 μmol/L; 24 h) modulates apoptosis and cell cycle-related protein expression in H1650 non-small cell lung cancer cells, reducing cyclin D1, CDK4, and Bcl-2 and increasing Bax, cleaved-caspase 3, cleaved-caspase 9, and cytochrome C[1].
Sotetsuflavone (64-128 μmol/L; 24 h) induces G0/G1 phase cell cycle arrest in H1650 non-small cell lung cancer cells[1].
Sotetsuflavone (64-128 μmol/L; 24 h) induces autophagy in A549 cells, as shown by increased LC3-II conversion and reduced P62 expression[1].
Sotetsuflavone (64-128 μmol/L; 24 h) increases autophagosome formation in A549 non-small cell lung cancer cells[1].
Sotetsuflavone (64-128 μmol/L; 24 h) increases the formation of acidic vesicle organelles in A549 non-small cell lung cancer cells, indicating enhanced autophagy[1].
Sotetsuflavone (5-200 μmol/L; 12-48 h) inhibits the proliferation of A549 cells in a time- and dose-dependent manner[2].
Sotetsuflavone (64-128 μmol/L; 24 h) dose-dependently increases intracellular ROS levels in A549 cells[2].
Sotetsuflavone (64-128 μmol/L; 24 h) dose-dependently reduces the mitochondrial membrane potential of A549 cells[2].
Sotetsuflavone (64-128 μmol/L; 24 h) dose-dependently modulates epithelial-mesenchymal transition marker proteins in human non-small-cell lung cancer A549 cells, increasing E-cadherin and decreasing Snail, HIF-1α, MMP-9/13, VEGF, TNF-α and NF-κB expression[3].
Sotetsuflavone (64-128 μmol/L; 24 h) dose-dependently inhibits PI3K and AKT expression in human non-small-cell lung cancer A549 cells, suppressing activation of the PI3K/AKT pathway[3].
Sotetsuflavone (64-128 μmol/L; 24 h) concentration-dependently downregulates STAT3, β-catenin, and TGF-β expression and upregulates ZO-1 expression in human non-small cell lung cancer A549 cells[4].
Sotetsuflavone (25-100 μM; 24 h) dose-dependently inhibits LPS (HY-D1056) plus IFN-γ-induced JNK and p38 phosphorylation in RAW264.7 macrophages[5].
Sotetsuflavone (50 μM; 12 h pre-incubation) inhibits the LPS plus IFN-γ-induced upregulation of M1 macrophage marker genes iNOS and IRF-5 in RAW264.7 macrophages, an effect mediated via suppression of p38 signalling[5].
Sotetsuflavone (50 μM; 12 h pre-incubation) protects mouse colonic organoids from M1 macrophage-induced damage, including reduced size, impaired budding, and increased permeability, via suppression of p38 and JNK signalling[5].

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

Sotetsuflavone Related Antibodies

Western Blot Analysis[1]

Cell Line: A549 and H1650 non-small cell lung cancer cells
Concentration: 64; 128 μmol/L
Incubation Time: 24 h
Result: Reduced the phosphorylation levels of PI3K, Akt, mTOR, Raptor, and p70S6K in A549 cells.
Significantly increased LC3-II conversion and reduced P62 expression in both A549 and H1650 cells when co-treated with 20 μM LY294002 (HY-10108).

Cell Viability Assay[1]

Cell Line: H1650 non-small cell lung cancer cells
Concentration: 5; 10; 20; 40; 80; 100; 120; 160; 200 μmol/L
Incubation Time: 24 h
Result: Inhibited H1650 cell growth in a dose- and time-dependent manner.
Exhibited an IC50 value of 67.54 μmol/L.

Cell Proliferation Assay[1]

Cell Line: A549 and H1650 non-small cell lung cancer cells
Concentration: 64; 128 μmol/L
Incubation Time: 14 days
Result: Reduced A549 cell colony numbers to ~35% and ~15% of control at 64 and 128 μmol/L, respectively.
Reduced H1650 cell colony numbers to ~30% and ~10% of control at 64 and 128 μmol/L, respectively.

Cell Migration Assay [1]

Cell Line: H1650 non-small cell lung cancer cells
Concentration: 64; 128 μmol/L
Incubation Time: 24 h
Result: Reduced H1650 cell migration to ~55% and ~35% of control at 64 and 128 μmol/L, respectively.

Cell Cycle Analysis[1]

Cell Line: H1650 non-small cell lung cancer cells
Concentration: 64; 128 μmol/L
Incubation Time: 24 h
Result: Increased the proportion of H1650 cells in the G0/G1 phase and decreased the proportion in the G2/M phase compared to control.

Cell Proliferation Assay[2]

Cell Line: human non-small cell lung cancer A549 cells
Concentration: 5; 10; 20; 40; 80; 100; 120; 160; 200 μmol/L
Incubation Time: 12; 24; 48 h
Result: Inhibited A549 cell proliferation in a time- and dose-dependent manner.
Reduced cell viability significantly at concentrations ≥80 μmol/L across all incubation times.
Showed no significant difference in inhibitory effect between 12 h, 24 h, and 48 h at concentrations >80 μmol/L.
Exhibited IC50 values of 87 μmol/L for 12 h incubation, 71 μmol/L for 24 h incubation, and 63 μmol/L for 48 h incubation.

Apoptosis Analysis[2]

Cell Line: human non-small cell lung cancer A549 cells
Concentration: 64; 128 μmol/L
Incubation Time: 24 h
Result: Induced apoptosis in A549 cells in a dose-dependent manner.
Increased the apoptosis ratio from a low control level to ~10% at 64 μmol/L and ~32% at 128 μmol/L.
Increased green (Annexin V-FITC) and red (PI) staining with higher sotetsuflavone concentrations.\nIncreased the number of cells with condensed, fragmented bright blue nuclei (apoptotic cells) in a dose-dependent manner.

Western Blot Analysis[2]

Cell Line: human non-small cell lung cancer A549 cells
Concentration: 64; 128 μmol/L
Incubation Time: 24 h
Result: Downregulated cell cycle-related proteins Cyclin D1 and CDK4 in a dose-dependent manner.
Upregulated pro-apoptotic proteins Bax, cleaved caspase-3, cleaved caspase-9, and cytochrome C in a dose-dependent manner.
Downregulated anti-apoptotic protein Bcl-2 and death receptor pathway protein cleaved caspase-8 in a dose-dependent manner.
Increased the Bax/Bcl-2 ratio.

Western Blot Analysis[3]

Cell Line: human non-small-cell lung cancer A549 cells
Concentration: 64; 128 μmol/L
Incubation Time: 24 h
Result: Upregulated E-cadherin protein expression in a dose-dependent manner compared to the control group.
Downregulated Snail protein expression in a dose-dependent manner compared to the control group.

Real Time qPCR[3]

Cell Line: human non-small-cell lung cancer A549 cells
Concentration: 64; 128 μmol/L
Incubation Time: 24 h
Result: Downregulated mRNA expression of Snail in a dose-dependent manner compared to the control group.
Downregulated mRNA expression of Vimentin in a dose-dependent manner compared to the control group.
Downregulated mRNA expression of N-cadherin in a dose-dependent manner compared to the control group.

Immunofluorescence[4]

Cell Line: human non-small cell lung cancer A549 cells
Concentration: 64; 128 μmol/L
Incubation Time: 24 h
Result: Significantly increases endostatin fluorescence intensity and significantly decreases TGF-β fluorescence intensity compared to control at 64 μmol/L.
Produces a further significant increase in endostatin fluorescence intensity and further significant decrease in TGF-β fluorescence intensity compared to control at 128 μmol/L, with effects showing a concentration-dependent trend.
Localizes endostatin primarily to the A549 cell membrane, while TGF-β is localized primarily to the cytoplasm.

Real Time qPCR[4]

Cell Line: human non-small cell lung cancer A549 cells
Concentration: 64; 128 μmol/L
Incubation Time: 24 h
Result: Significantly decreased STAT3, β-catenin, and TGF-β mRNA expression, and significantly increases ZO-1 mRNA expression compared to control at 64 μmol/L.
Produces a further significant decrease in STAT3, β-catenin, and TGF-β mRNA expression, and further significant increase in ZO-1 mRNA expression compared to control at 128 μmol/L, with effects showing a concentration-dependent trend.

Western Blot Analysis[4]

Cell Line: human non-small cell lung cancer A549 cells
Concentration: 64; 128 μmol/L
Incubation Time: 24 h
Result: Significantly decreases STAT3 and β-catenin protein expression relative to GAPDH compared to control at 64 μmol/L.
Produces a further significant decrease in STAT3 and β-catenin protein expression relative to GAPDH compared to control at 128 μmol/L, with effects showing a concentration-dependent trend.

Western Blot Analysis[5]

Cell Line: RAW264.7 macrophages
Concentration: 25; 50; 100 μM
Incubation Time: 24 h
Result: Dose-dependently inhibited the LPS (HY-D1056) plus IFN-γ-induced increases in phosphorylated JNK (p-JNK) and phosphorylated p38 protein levels.
Reduced relative p-JNK protein to ~2.7-fold and relative p-p38 protein to ~2.5-fold at 25 μM compared to the non-stimulated control group's ~1-fold.
Reduced relative p-JNK protein to ~1.5-fold and relative p-p38 protein to ~1.5-fold at 50 μM.
Reduced relative p-JNK protein to ~1.2-fold and relative p-p38 protein to ~1.2-fold at 100 μM.

Real Time qPCR[5]

Cell Line: RAW264.7 macrophages
Concentration: 50 μM
Incubation Time: 12 h pre-incubation, followed by 24 h LPS/IFN-γ stimulation
Result: Down-regulated the transcript levels of M1 macrophage genes iNOS and IRF-5 in LPS plus IFN-γ-induced RAW264.7 cells.
Reduced relative iNOS mRNA from ~2.5-fold (LPS/IFN-γ only) to ~1.7-fold compared to the non-stimulated control group's ~1-fold.
Reduced relative IRF5 mRNA from ~3.8-fold (LPS/IFN-γ only) to ~1.7-fold compared to the non-stimulated control group's ~1-fold.
Inhibitory effect was abolished by co-treatment with the p38 agonist anisomycin (50 nM).
In Vivo

Sotetsuflavone (20-40 mg/kg; i.p.; every 4 days; 28 days) inhibits non-small cell lung cancer xenograft growth in BALB/C nude mice[1].
Sotetsuflavone (40 mg/kg; i.p.; every other day; 4 weeks) ameliorates spontaneous Crohn's disease-like colitis in IL-10-/- mice[5].

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

Animal Model: BALB/C mice (male, 4 weeks old) subcutaneously inoculated with A549 cells[1]
Dosage: 20; 40 mg/kg
Administration: i.p.; every 4 days; 28 days
Result: Significantly reduced tumor volume and mean tumor weight relative to control.
Resulted in lower mean tumor weight at 40 mg/kg dose than at 20 mg/kg dose.
Increased apoptotic cells in tumor tissues, with more apoptosis observed in the 40 mg/kg group.
Increased LC3 expression and decreased P62 expression in tumor tissues.
Maintained stable mouse body weight throughout the study.
Showed no serious morphological changes in lung, intestine, or liver tissues.
Animal Model: IL-10-/- mice (15-week-old male) with colitis[5]
Dosage: 40 mg/kg
Administration: i.p.; every other day; 4 weeks
Result: Significantly reduced disease activity index (DAI) scores starting 2 weeks post-treatment.
Increased net weight change relative to untreated IL-10-/- mice.
Attenuated colon shortening.
Reduced macroscopic colonic mucosal injury scores to 3.63 and colonic inflammatory scores to 2.
Lowered serum intestinal fatty acid binding protein (I-FABP) levels and blood FITC-dextran levels.
Increased transepithelial electric resistance (TEER) of colon tissues.
Reduced bacterial translocation rate to mesentery lymph nodes (MLNs) from 37.25% to 12.5% and to liver from 31.25% to 6.25%.
Decreased the percentage of iNOS+/F4/80+ M1 macrophages from 7.69% to 3.89%, increased the percentage of CD206+/F4/80+ M2 macrophages from 8.91% to 13.14%, and reduced the M1/M2 ratio.
Decreased protein and mRNA levels of proinflammatory cytokines TNF-α, IL-6, IFN-γ, and IL-1β.
Inhibited phosphorylation of JNK and p38 in intestinal epithelial macrophages.
Molecular Weight

552.48

Formula

C31H20O10
CAS No.
Appearance

Solid

Color

Light brown to brown

SMILES

O=C1C=C(C2=CC=C(O)C=C2)OC3=C(C4=CC(C5=CC(C6=C(O)C=C(O)C=C6O5)=O)=CC=C4O)C(OC)=CC(O)=C13
Structure Classification
Initial Source
Shipping

Room temperature in continental US; may vary elsewhere.
Storage

4°C, protect from light

*In solvent : -80°C, 6 months; -20°C, 1 month (protect from light)

Purity & Documentation
References
  • No file chosen (Maximum size is: 1024 Kb)
  • If you have published this work, please enter the PubMed ID.
  • Your name will appear on the site.

Sotetsuflavone Related Classifications

  • Molarity Calculator

  • Dilution Calculator

The molarity calculator equation

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

Mass   Concentration   Volume   Molecular Weight *
= × ×

The dilution calculator equation

Concentration (start) × Volume (start) = Concentration (final) × Volume (final)

This equation is commonly abbreviated as: C1V1 = C2V2

Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
× = ×
C1   V1   C2   V2
Help & FAQs
  • Do most proteins show cross-species activity?

    Species cross-reactivity must be investigated individually for each product. Many human cytokines will produce a nice response in mouse cell lines, and many mouse proteins will show activity on human cells. Other proteins may have a lower specific activity when used in the opposite species.

Keywords:

Sotetsuflavone2608-21-1ApoptosisAutophagyPI3KJNKmTORp38 MAPKCDKMMPTGF-beta/SmadSTATβ-cateninReactive Oxygen Species (ROS)Bcl-2 FamilyCaspasePhosphoinositide 3-kinasec-Jun N-terminal kinaseMammalian target of RapamycinCyclin dependent kinaseMatrix metalloproteinasesTransforming growth factor betaBeta cateninnon-small cell lung cancerTNF-α/NF-κB pathwayCrohn’s diseaseA549 cellsPI3K/Akt/mTOR pathwayBEAS-2B cellsRAW264.7 macrophagesautophagyepithelial-mesenchymal transitionH1650 cellsInhibitorinhibitorinhibit

Your Recently Viewed Products:

Inquiry Online

Your information is safe with us. * Required Fields.

Product Name

  

Requested Quantity *

Applicant Name *

 

Salutation

Email Address *

 

Phone Number *

Department

 

Organization Name *

City

State

Country or Region *

      

Remarks

Bulk Inquiry

Inquiry Information

Product Name:
Sotetsuflavone
Cat. No.:
HY-N2199
Quantity:
MCE Japan Authorized Agent:

Customer Review

Thank You for Your Feedback!

Request for HNMR Report

Please fill out this form to request the QC report. We will send it to your Email address shortly.

Your information is safe with us. * Required Fields.

Product Name

  

Lot #

Applicant Name *

 

Email Address *

Phone Number

 

Department *

Organization Name *

 

Country or Region *

Remarks

SAFETY DATA SHEET (SDS)

English - EN (252 KB) Français - FR (252 KB) Deutsch - DE (252 KB) Norwegian - NO (252 KB) Español - ES (252 KB) Swedish - SV (252 KB) Italian - IT (252 KB) Korean - KR (252 KB) Portuguese - PT (252 KB)

Request for HNMR Report

We have received your request and will respond to you as soon as possible.