2. Others Stem Cell/Wnt JAK/STAT Signaling Cell Cycle/DNA Damage Epigenetics PI3K/Akt/mTOR Metabolic Enzyme/Protease
  3. Drug Derivative STAT Sirtuin AMPK PAI-1 MicroRNA Akt Mitochondrial Metabolism
  4. Mito-Esculetin

Mito-Esculetin (Mito-Esc) is an orally active mitochondria-targeted derivative of Esculetin (HY-N0284). Mito-Esculetin inhibits LPS-induced phosphorylation of STAT3 Tyr-705, partially reverses LPS-mediated depletion of SIRT3, and enhances the AMPK-SIRT1 signaling axis. Mito-Esculetin inhibits PAI-1 activity, regulates miRNA, and induces phosphorylation of IRS and AKT. Mito-Esculetin suppresses oxidant-induced endothelial dysfunction, Ang-II (HY-13948)- and high glucose-induced atherosclerotic plaque formation, Palmitate (HY-N0830)-induced insulin resistance, as well as high glucose-mediated endothelial cell senescence and inflammatory responses. Mito-Esculetin reduces body weight and non-esterified fatty acid (NEFA) levels. Mito-Esculetin can be used in research related to acute coronary syndrome, type 2 diabetes, and hyperglycemia-induced atherosclerosis.

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

Mito-Esculetin

Mito-Esculetin Chemical Structure

CAS No. : 1993461-76-9

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.

Mito-Esculetin Related Antibodies

Top Publications Citing Use of Products

View All STAT Isoform Specific Products:

View All Isoforms
STAT3 STAT5 STAT6 STAT1

View All Sirtuin Isoform Specific Products:

View All Isoforms
Sirtuin SIRT1 SIRT2 SIRT3 SIRT6 SIRT5 SIRT7 SIRT4

View All AMPK Isoform Specific Products:

View All Isoforms
NUAK1 NUAK2 AMPK AMPK α1β1γ1 AMPK α2β1γ1 AMPK α1β2γ1 AMPK α2β2γ1 BRSK1 BRSK2 HUNK AMPKα

View All Akt Isoform Specific Products:

View All Isoforms
Akt Akt1 Akt2 Akt3

  • Biological Activity

  • Purity & Documentation

  • References

  • Customer Review

Description

Mito-Esculetin (Mito-Esc) is an orally active mitochondria-targeted derivative of Esculetin (HY-N0284). Mito-Esculetin inhibits LPS-induced phosphorylation of STAT3 Tyr-705, partially reverses LPS-mediated depletion of SIRT3, and enhances the AMPK-SIRT1 signaling axis. Mito-Esculetin inhibits PAI-1 activity, regulates miRNA, and induces phosphorylation of IRS and AKT. Mito-Esculetin suppresses oxidant-induced endothelial dysfunction, Ang-II (HY-13948)- and high glucose-induced atherosclerotic plaque formation, Palmitate (HY-N0830)-induced insulin resistance, as well as high glucose-mediated endothelial cell senescence and inflammatory responses. Mito-Esculetin reduces body weight and non-esterified fatty acid (NEFA) levels. Mito-Esculetin can be used in research related to acute coronary syndrome, type 2 diabetes, and hyperglycemia-induced atherosclerosis[1][2].

In Vitro

Mito-Esculetin (10 μM; 10 min) inhibits the activity of recombinant PAI-1 in cell-free biochemical assays[1].
Mito-Esculetin (2.5 μM; 2 h pretreatment) significantly inhibits PAI-1 activity and mRNA expression in lipopolysaccharide (LPS)-induced human aortic endothelial cells (HAECs), and its efficacy is stronger than that of the parent compound Esculetin (HY-N0284)[1].
Mito-Esculetin (2.5 μM; 2 h) inhibits lipopolysaccharide (LPS)-induced phosphorylation of STAT3Tyr-705 in human aortic endothelial cells (HAECs)[1].
Mito-Esc (1.25 μM; 6 h) inhibits gluconeogenesis, restores the insulin signaling pathway, enhances glucose uptake, and promotes GLUT4 translocation in palmitate-induced insulin-resistant HepG2 cells[2].
Mito-Esc (1.25 μM; 1 h pre-incubation) inhibits high glucose-induced adhesion between monocytes and HAEC[2].
Mito-Esc (1.25 μM; 1 h pre-incubation) attenuates high glucose-induced senescence and oxidative stress, restores the AMPK-eNOS-SIRT1 signaling pathway in HAECs, and this effect depends on functionally intact AMPK and SIRT1[2].

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

Mito-Esculetin Related Antibodies

ELISA Assay[1]

Cell Line: Human aortic endothelial cells (HAECs)
Concentration: 2.5 μM
Incubation Time: 2 h pretreatment, followed by 4 h LPS co-incubation
Result: Significantly inhibited LPS-induced PAI-1 activity in conditioned medium.
Significantly reduced LPS-induced PAI-1 transcript levels.
Exerted a more pronounced inhibitory effect than parent esculetin.

Western Blot Analysis[1]

Cell Line: Human aortic endothelial cells (HAECs)
Concentration: 2.5 μM
Incubation Time: 2 h pretreatment, followed by 4 h LPS co-incubation
Result: Greatly inhibited LPS-induced increases in phospho-STAT3 (Tyr-705) protein levels.
In Vivo

Mito-Esculetin (0.5 mg/kg; p.o.; daily; 2 months) significantly attenuates Ang-II-induced PAI-1 and miR-19b levels while restoring miR-30c levels in ApoE-/- mice with atherosclerosis[1].
Mito-Esculetin (0.312-1.25 mg/kg; p.o.; daily; 30 days) administered orally to db/db mice dose-dependently improves glucose homeostasis, insulin resistance, liver function, adipose tissue health, and hyperglycemia-induced atherosclerosis by reducing inflammation, senescence, and oxidative stress, with the 1.25 mg/kg dose showing the greatest efficacy[2].

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

Animal Model: ApoE-/- (2-month-old male, Angiotensin II-induced atherosclerosis)[1]
Dosage: 0.5 mg/kg
Administration: p.o.; daily; 2 months
Result: Significantly inhibited Ang-II-induced plasma PAI-1 levels.
Repressed Ang-II-mediated elevation of aortic miR-19b levels.
Restored Ang-II-reduced aortic miR-30c levels.
Animal Model: db/db (4-month-old male/female; spontaneous hyperglycemia, insulin resistance, dyslipidemia)[2]
Dosage: 0.312 mg/kg; 0.625 mg/kg; 1.25 mg/kg
Administration: p.o.; daily; 30 days
Result: Significantly reduced fasting and random blood glucose levels, and HbA1c levels relative to db/db controls.
Normalized serum insulin levels, and increased the quantitative insulin sensitivity check (QUICK) index dose-dependently.
Dose-dependently improved liver tissue morphology, reduced serum AST and ALT levels, decreased liver LDL-cholesterol and triglyceride levels, increased liver glycogen content, inhibited liver fructose-1,6-bisphosphatase (FBPase) activity, and reduced liver non-esterified free fatty acid (NEFA) levels relative to db/db controls.
Dose-dependently reduced adipocyte hypertrophy and lipid accumulation in adipose tissue relative to db/db controls, with greater reduction than simvastatin and pioglitazone.
Dose-dependently reduced aortic lesion area, collagen accumulation, and lipid accumulation relative to db/db controls; 0.625 and 1.25 mg/kg doses showed greater reduction than simvastatin and pioglitazone.
Significantly reduced serum LDL-cholesterol and triglyceride levels dose-dependently, while HDL levels were unchanged.
Significantly reduced mean arterial blood pressure.
Dose-dependently reduced aortic VCAM-1, ICAM-1, and MAC3 expression, normalized M1/M2 macrophage marker transcript levels in aorta, and reduced serum TNF-α, IL-1β, IL-6, IL-10, and MCP-1 levels relative to db/db controls; the 1.25 mg/kg dose showed greater reduction in TNF-α, IL-6, and MCP-1 than simvastatin and pioglitazone.
Dose-dependently reduced aortic transcript levels of senescence markers p16, p21, p27, and p53, restored aortic phospho-AMPK, phospho-eNOS, and SIRT1 protein levels, and increased serum GSH and nitrite/nitrate levels relative to db/db controls.
Molecular Weight

631.54

Formula

C35H36BrO4P
CAS No.
SMILES

O=C1OC2=C(C(CCCCCCCC[P+](C3=CC=CC=C3)(C4=CC=CC=C4)C5=CC=CC=C5)=C1)C=C(O)C(O)=C2.[Br-]
Shipping

Room temperature in continental US; may vary elsewhere.
Storage

Please store the product under the recommended conditions in the Certificate of Analysis.
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.

Mito-Esculetin 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:

Mito-Esculetin1993461-76-9Mito-EscDrug DerivativeSTATSirtuinAMPKPAI-1MicroRNAAktMitochondrial MetabolismDrug derivativeAMP-activated protein kinasePlasminogen activator inhibitor-1miRNAPKBProtein kinase BAMPK-SIRT1 axisSTAT3 Tyr-705 phosphorylationSIRT33T3-L1 pre-adipocytesdb/db micehuman aortic endothelial cellsHepG2 cellsApoE-/- micetype 2 diabetesInhibitorinhibitorinhibit

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:
Mito-Esculetin
Cat. No.:
HY-184265
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)

Request for HNMR Report

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