12-HETE

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.