4 hydroxynonenal

4-Hydroxynonenal (4-HNE) 是一种 α，β 不饱和羟基烯醛，可作为氧化 亚硝化应激生物标志物。它是ALDH2的底物和抑制剂。它可以调节许多信号传导过程，主要是通过与蛋白质，核酸和膜脂质中具有亲核官能团的共价加合物形成的。它通过线粒体在癌症中起重要作用。

4-Hydroxynonenal BSA 是 4-Hydroxynonenal 与 牛血清白蛋白 (BSA) 的抗原-佐剂偶联物。抗原与蛋白佐剂的结合能够提高模型中抗原特异性抗体的生成。此缀合物不影响蛋白质折叠或破坏主要表位，并且促进交叉呈递和抗原特异性 T 细胞的生成。

4-hydroxy Nonenal (4-HNE) is a major aldehyde produced during the lipid peroxidation of ω-6 polyunsaturated fatty acids, such as arachidonic acid and linoleic acid. It is considered a potential causal agent in numerous diseases, including chronic inflammation, neurodegenerative diseases, atherosclerosis, diabetes, and cancer, in part because it covalently modifies DNA and proteins resulting in genetic mutations and altered cell signaling, respectively. 4-HNE Alkyne is a form of 4-HNE with a terminal alkyne. Such terminal alkyne groups can be used in linking reactions, known as click chemistry, characterized by high dependability and specificity of azide-alkyne bioconjugation reactions. Click chemistry has only recently been applied to the study of oxidized lipids.

Peroxidation of common ω-6 polyunsaturated fatty acids (PUFAs) such as linoleic acid, DGLA, and arachidonic acid can give rise to 4-HNE. 4-HNE is cleared rapidly from the plasma and undergoes enterohepatic circulation as a glutathione conjugate in the rat. About two thirds of an administered dose of 4-HNE is excreted within 48 hours in the urine, primarily in the form of mercapturic acid conjugates. The C-1 aldehyde of 4-HNE is reduced to an alcohol in about half of these metabolites. The remainder are C-1 aldehydes or have been oxidized to C-1 carboxylic acids. These aldehydes and carboxylic acids can also form γ-lactols and γ-lactones, respectively, producing at least 4 or 5 end urinary metabolites of 4-HNE in vivo.

Reproxalap (NS-2) 是一种活性醛类隔离剂，可用于干眼症的研究。它能够与醛 (包括丙二醛和 4-羟基壬醛) 共价结合。

KR-67607, also known as NTX-101 is novel selective 11β-hydroxysteroid dehydrogenase 1 (11β-HSD1) inhibitor. KR-67607 decreased 4-hydroxynonenal expression and increased antioxidant and mucus secretion in BAC-treated rat eyes. KR-67607 showed its protective effects against ischemia-reperfusion-induced eye injury. KR-67607 effectively reduced cortisol levels in mouse eyes and maintained the trabecular meshwork (TM) structure in the presence of transient ischemic stress. Furthermore, KR-67607 reversed the elevation of intra-ocular pressure (IOP), suggesting that the TM structure maintained by KR-67607 prevented the excessive rise in IOP that exacerbates glaucoma.