HET0016
20-HETE biosynthesis inhibitor / HET0016 (339068-25-6) inhibits 20-hydroxyeicosatetraenoic acid (20-HETE) biosynthesis via omega oxidation of arachidonic acid mediated by CYP4A and 4F (IC50=8.9 nM in human renal microsomes).1 It displays neuroprotective effects in a rat model of traumatic brain injury via inhibition of neuronal pyroptosis.2 HET0016 attenuates cerebral ischemia-reperfusion injury3 as well as oxidative injury and peripheral nerve damage in type-2 diabetic mice4. It alleviates myocardial oxidative stress5 and restores endothelial function suggesting therapeutic potential in obesity-associated vascular disease6.
Biochemicals & reagents
339068-25-6
1 Miyata et al. (2001), HET0016, a potent and selective inhibitor of 20-HETE synthesizing enzyme; Br. J. Pharmacol. 133 325 2 Chen et al. (2023), HET0016 inhibits neuronal pyroptosis in the immature brain post-TBI via the p38 MAPK signaling pathway; Neuropharmacology, 239 109687 3 Yang et al. (2020), N-hydroxy-N’-(4-butyl-2-methylphenyl)-formamidine attenuates oxygen-glucose deprivation and reoxygenation-induced cerebral ischemia-reperfusion injury via regulation of microRNAs; J. Integr. Neuroscience 19 303 4 Haddad et al. (2022), Activation of 20-HETE Synthase Triggers Oxidative Injury and Peripheral Nerve Damage in Type 2 Diabetic Mice; J. Pain 23 1371 5 Wang et al. (2019), Specific Inhibition of CYP4A Alleviates Myocardial Oxidative Stress and Apoptosis Induced by Advanced Glycation End-Products; Front. Pharmacol. 10 876 6 Munoz et al. (2022), Differential contribution of renal cytochrome P450 enzymes to kidney endothelial dysfunction and vascular oxidative stress in obesity; Biochem. Pharmacol. 195 114850
-20°C
TARGET: Cytochrome/MDR -- PATHWAY: Pyroptosis; Fatty acid metabolism -- RESEARCH AREA: Neuroscience; Oxidative stress; Cell death -- DISEASE AREA: Neurodegeneration; IschemiaHeart disease