non-enzymatic

7α-Hydroxycholesterol 是一种由酶促氧化和非酶促氧化形成的胆固醇氧化物，可用作脂质过氧化的生物标志物。

5-A-RU (5-Amino-6-(D-ribitylamino)uracil)是核黄素生物合成的早期中间体，存在于多种细菌和酵母以及植物中。5-A-RU也是一种粘膜相关不变 T （MAIT） 细胞激活剂，通过与来自其他代谢途径的小分子的非酶促反应形成有效的MAIT激活抗原。

Etravirine (R165335) 是一种非核苷逆转录酶抑制剂，具有抗 HIV 的作用。

LV-320 是一种有效且非竞争性的ATG4B 抑制剂，其IC50值为 24.5 μM，Kd 值为 16 μM。 LV-320 抑制ATG4B 的酶促活性，阻断细胞自噬，并且稳定无毒，在体内具有活性。

EP652 (compound 56) 在抑制METTL3酶活性方面表现出高效能，其在SPA、细胞内和ATPlite测定中的IC50分别为2 nM、< 10 nM和37 nM。EP652 对非实体和实体肿瘤研究具有重要意义。

Quinapril是一种可口服的非肽和非巯基血管紧张素转换酶（ACE）抑制剂。它专门阻止血浆与组织中的血管紧张素I向血管紧张素II的转换。Quinapril通过酶水解生成具有药理活性的Quinaprilat，对高血压模型具有疗效。

Secoisolariciresinol diglucoside (LGM2605) 在铁过载诱导的氧化还原炎症损伤的体外模型中具有细胞保护作用。 Secoisolariciresinol Diglucoside(25 mg kg b.w.) 通过抑制 ROS 水平介导的酶和非酶抗氧化剂水平升高来防止肝脏受到过氧化损伤，从而发挥抗高血糖作用。

(±)11-HETE is one of the six monohydroxy fatty acids produced by the non-enzymatic oxidation of arachidonic acid . The individual R and S isomers of racemic HETEs have been separated and identified using chiral phase HPLC. The racemic HETEs have been quantified as an index of lipid peroxidation using GC/MS.

(±)18-HEPE is produced by non-enzymatic oxidation of EPA. It contains equal amounts of 18(S)-HEPE and 18(R)-HEPE. Specific biological activity attributed to (±)18-HEPE has not been documented.

(±)12-HEPE is produced by non-enzymatic oxidation of EPA. It contains equal amounts of 12(S)-HEPE and 12(R)-HEPE. The biological activity of (±)12-HEPE is likely mediated by one of the individual isomers, most commonly the 12(S) isomer in mammalian systems. 12-HEPE inhibits platelet aggregation with the same potency as 12-HETE, exhibiting IC50 values of 24 and 25 µM, respectively. [1] These compounds are also equipotent as inhibitors of U46619-induced contraction of rat aorta (IC50s = 8.6-8.8 µM).[2]

(±)14-HDHA是一种羟基二十二碳六烯酸，是DHA在细胞内通过酶促或非酶促反应生成的氧化代谢物，是15-PGDH的特异性底物之一并且可以被进一步氧化为具有抗炎性的14-oxoDHA，在原代肺泡巨噬细胞中，14-HDoHE 本身也能显著抑制 LPS 诱导的 IL-6 mRNA 表达，可能与哮喘等炎症性疾病有关。

(±)15-HEDE is produced by non-enzymatic oxidation of 11,14-eicosadienoic acid. There are no reports in the literature of biological activity associated with (±)15-HEDE.

Advanced glycation end products (AGEs) are compounds formed by non-enzymatic chemical reactions following the bonding of sugars to proteins or lipids during diabetes, uremia, aging, rheumatic arthritis, and other conditions. A receptor for the AGEs (RAGE) binds certain members of this class to initiate cell signaling.[1][2] Pentosidine is a well-characterized natural AGE that is often used as a biomarker for the production of all AGEs. While pentosidine can be measured in urine, the majority of this AGE is catabolized before excretion.[3] Reference：[1]. Neeper, M., Schmidt, A.M., Brett, J., et al. Cloning and expression of a cell surface receptor for advanced glycosylation end products of proteins. The Journal of Biological Chemisty 267(21), 14998-15004 (1992).[2]. Brett, J., Schmidt, A.M., Yan, S.D., et al. Survey of the distribution of a newly characterized receptor for advanced glycation end products in tissues. American Journal of Pathology 143(6), 1699-1712 (1993).[3]. Miyata, T., Ueda, Y., Horie, K., et al. Renal catabolism of advanced glycation end products: The fate of pentosidine. Kidney International 53, 416-422 (1998).

Isoprostanes are produced by the non-enzymatic, free radical peroxidation of phospholipid-esterified arachidonic acid. They have been used as biomarkers of oxidative stress, but they also have been found to have potent biological activity. ent-8-iso-15(S)-Prostaglandin F2α (ent-8-iso-15(S)-PGF2α) is a potent vasoconstrictor of porcine retinal and brain microvessels with EC50 values of 15 and 24 nM, respectively. This isoprostane is about ten-fold more potent than 8-iso-PGF2α in a whole blood platelet aggregation inhibition assay.

8-iso Prostaglandin F2β (8-iso PGF2β) is an isomer of PGF2α of non-enzymatic origin. It is one of 64 possible isomers of PGF2α which can be produced by free radical peroxidation of arachidonic acid. 8-iso PGF2β exhibits very weak contraction of human umbilical vein artery and does not promote aggregation of human whole blood. However, 8-iso PGF2β moderately contracts both the canine and porcine pulmonary vein, although the effect is much weaker than that exhibited by other isoprostanes such as 8-iso PGE1, 8-iso PGE2, or 8-iso PGF2α. 8-iso-15-keto PGF2β is a potential metabolite of 8-iso PGF2β via the 15-hydroxy PG dehydrogenase pathway. There are no published reports on the formation or biological activity of 8-iso-15-keto PGF2β.

Prostaglandin B2 (PGB2) is a non-enzymatic dehydration product resulting from the treatment of PGE2 or PGA2 with strong base. It has weak agonist activity on TP receptors and can increase pulmonary blood pressure in the rabbit at relatively high doses (5 ug kg). [1]

(±)9-HETE is one of the six monohydroxy fatty acids produced by the non-enzymatic oxidation of arachidonic acid. The individual R and S isomers of racemic HETEs have been separated and identified using chiral phase HPLC. The racemic HETEs have been quantified as an index of lipid peroxidation using GC MS.

(±)9-HODE is one of the two racemic monohydroxy fatty acids resulting from the non-enzymatic oxidation of linoleic acid. Approximately equal proportions of both isomers are found in mitochondrial and plasma membranes of rabbit reticulocytes. [1][2] Oxidized LDL contains significant amounts of esterified 9- and 13-HpODEs and HODEs. [3][4]

(±)5-HEPE is produced by non-enzymatic oxidation of EPA. It contains equal amounts of 5(S)-HEPE and 5(R)-HEPE. The biological activity of (±)5-HEPE is likely mediated by one of the individual isomers, most commonly the 5(S) isomer in mammalian systems. EPA can be metabolized to 5-HEPE in human and bovine neutrophils, and human eosinophils, which is further metabolized to 5-oxoEPE and LTB5. The 5-series metabolites of EPA, namely 5-HEPE, 5-oxoEPE, and LTB5, have significantly decreased biological effects compared to the arachidonic acid-derived metabolites.

(±)8-HEPE is produced by non-enzymatic oxidation of EPA. It contains equal amounts of 8(S)-HEPE and 8(R)-HEPE. The ability of (±)8-HEPE to induce hatching of E. modestus and B. balanoides eggs is probably due to the presence of the 8(R) isomer within the racemic mixture.[1][2] Reference：[1]. Shing, T.K.M., Gibson, K.H., Wiley, J.R., et al. First total synthesis of a barnacle hatching factor 8(R)-hydroxy-eicosa-5(Z),9(E),11(Z)-pentaenoic acid. Tetrahedron Letters 35, 1067-1070 (1994).[2]. Hill, E.M., and Holland, D.L. Identification and egg hatching activity of monohydroxy fatty acid eicosanoids in the barnacle Balanus balanoides. Proceedings of the Royal Society of London Series B.Biological Sciences 247, 41-46 (1991).

(±)9-HEPE is produced by non-enzymatic oxidation of EPA. It contains equal amounts of 9(S)-HEPE and 9(R)-HEPE. The biological activity of (±)9-HEPE has not been clearly documented.

(±)13-HODE is one of the two racemic monohydroxy fatty acids resulting from the non-enzymatic oxidation of linoleic acid. It is the principle hydroxylated fatty acid in human psoriatic skin scales, with a mean concentration of 17 ng/mg.[1]

Pravastatin lactone is a metabolite of pravastatin , a hydroxymethylglutaryl-coenzyme A (HMG-CoA) reductase inhibitor that is a ring-hydroxylated metabolite of mevastatin . Pravastatin lactone is formed when pravastatin undergoes acid-catalyzed non-enzymatic lactonization in the stomach following oral administration.

5(S),6(S)-DiHETE is one of the four diastereomeric 5,6-dihydroxy acids produced from the non-enzymatic hydrolysis of LTA4. 5(S),6(S)-DiHETE does not have significant leukotriene-like activity.