2. Apoptosis
  3. Apoptosis
  4. 12-HETE

12-HETE, a major metabolic product of arachidonic acid using 12-LOX catalysis, inhibits cell apoptosis in a dose-dependent manner. 12-HETE promotes the activation and nuclear translocation of NF-κB through the integrin-linked kinase (ILK) pathway.12-HETE has both anti-thrombotic and pro-thrombotic effects. 12-HETE is a neuromodulator.

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

12-HETE Chemical Structure

12-HETE Chemical Structure

CAS No. : 71030-37-0

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50 μg（312.04 μM * 0.5 mL in Ethanol） USD 330 In-stock
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100 μg（312.04 μM * 1 mL in Ethanol） USD 540 In-stock
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Based on 1 publication(s) in Google Scholar

Other Forms of 12-HETE:

12-HETE Related Antibodies

Top Publications Citing Use of Products

1 Publications Citing Use of MCE 12-HETE

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Description

12-HETE, a major metabolic product of arachidonic acid using 12-LOX catalysis, inhibits cell apoptosis in a dose-dependent manner. 12-HETE promotes the activation and nuclear translocation of NF-κB through the integrin-linked kinase (ILK) pathway[1].12-HETE has both anti-thrombotic and pro-thrombotic effects[2]. 12-HETE is a neuromodulator[3].

In Vitro

12-HETE participates in the inhibition of cell apoptosis by activating the ILK/NF-κB pathway, implying an important underlying mechanism that promotes the survival of ovarian cancer cells. 12-HETE facilitates cell survival by activating the integrin-linked kinase/NF-κB pathway in ovarian cancer. 12-HETE protects against cell apoptosis in ovarian cancer cells in a concentration-dependent manner. 12-HETE (1 µM) significantly decreases the activation of caspase-3 induced by serum deprivation (SD).12-HETE represses the increased activity of caspase-3 induced by SD in a concentration-dependent manner, with an IC50 value of 1.13 µM[1].
12-HETE (1 µM) facilitates the activation and nuclear translocation of NF-κB via ILK in ovarian cancer cells[1].
12-HETE inhibits insulin secretion, reduces metabolic activity and induces cell death in human islets. 12-HETE increases bovine platelet aggregation induced by thrombin and inhibits prostaglandin E1-induced elevation of intracellular cAMP levels. 12-HETE inhibits washed platelet (WP) aggregation[2].
The neuronal effects of 12-HETE include attenuation of calcium influx and glutamate release as well as inhibition of AMPA receptor (AMPA-R) activation[3].

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

12-HETE Related Antibodies

Cell Viability Assay[1]

Cell Line: Ovarian cancer OVCAR-3 and SKOV3 cells
Concentration: 0, 0.2, 0.5, and 1 µM
Incubation Time: 0, 24, 48, 72, and 96 hours
Result: Inhibited the decrease in cell viability induced by SD in a dose-dependent manner.
1 µM 12-HETE treatment significantly mitigated the decrease in cell viability under conditions of SD.

Western Blot Analysis[1]

Cell Line: Ovarian cancer OVCAR-3 and SKOV3 cells
Concentration: 1 µM
Incubation Time:
Result: Led to increased levels of NF-κB p65 phosphorylation.
Caused a significant increase in the protein levels of nuclear NF-κB p65, which was accompanied by decreased levels of NF-κB p65 in the cytoplasm.
Molecular Weight

320.47

Formula

C20H32O3
CAS No.
Appearance

Liquid

Color

Colorless to light yellow

SMILES

CCCCC/C=C\CC(O)/C=C/C=C\C/C=C\CCCC(O)=O
Shipping

Room temperature in continental US; may vary elsewhere.
Storage

Solution, -20°C, 2 years
Purity & Documentation

Purity: 95.70%

COA (238 KB)

Handling Instructions (2659 KB)
References
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12-HETE Related Classifications

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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:

12-HETE71030-37-0ApoptosisHydroxyeicosatetraenoicacidlipoxygenaseischemiaAMPAeicosanoidG-proteinVSCCsglutamateexcitotoxicityILKapoptosisNF-κBovariancancerInhibitorinhibitorinhibit

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