15-lo

PD146176 (NSC-168807) 是一种 15-脂氧合酶(15-LO)抑制剂，抑制兔网织红细胞 15-LO，Ki 为 197 nM，IC50 为 0.54 μM。 它通过刺激老年三重转基因小鼠的自噬来逆转认知障碍、脑淀粉样变性和 tau 病理学。

Lonapalene (RS4317) 是一种 5-脂氧合酶 (5-LO) 抑制剂，具有抗银屑病的功效。Lonapalene 可局部阻断皮肤炎症。

9c(i472) is an inhibitor of 15-lipoxygenase-1 (15-LO-1; IC50 = 0.19 μM).1 It decreases LPS- and IFN-γ-induced NF- B activity in RAW-Blue cells when used at concentrations of 0.2, 1, and 5 μM. 9c(i472) reduces LPS- and IFN-γ-induced increases in Nos2 expression and lipid peroxidation in RAW 264.7 cells when used at a concentration of 5 μM.

h15-LOX-2 inhibitor 2 (Compound 10)，作为一种h15-LOX抑制剂，具有IC50值为26.9 μM及Ki值为16.4 μM。

h15-LOX-2 inhibitor 3 (Compound 13) 为一种h15-LOX抑制剂，表现出的IC50与Ki值分别为25 μM及15.1 μM。

COX-2 15-LOX-IN-6 (Compound 5l) 是一种同时抑制COX-2和15-LOX的抑制剂，其IC50分别为0.201 μM和11.723 μM。COX-2 15-LOX-IN-6 能有效抑制血清中的PGE、TNF-α、IL-6和iNOS表达，并在Carrageenan诱导的大鼠水肿模型中展现出抗炎活性。

COX-2 15-LOX-IN-1 (Compound 14) 是一种 COX-2 和 15-脂氧合酶 （15-LOX）抑制剂，可作用于 COX-1 (IC50: 10.65 μM)、COX-2 (IC50: 0.075 μM) 和 15-LOX (IC50: 2.98 μM)。COX-2-IN-25 具有抗炎作用。

h15-LOX-2 inhibitor 1（Comp 105）是一种针对人上皮细胞15-lipoxygenase-2 (h15-LOX-2)的抑制剂，表现出0.34 μM的IC50值。

COX-2 15-LOX-IN-2 作为一种效能高的双重抑制剂，对COX-2和15-LOX的IC50值分别为0.065 μM和1.86 μM，显示出显著的抗氧化活性。

COX-2 15-LOX-IN-3 (compound 5k) 为COX-2 15-LOX的一种双重抑制剂，具有分别为0.075 μM和1.97 μM的IC50值。该化合物能显著抑制LPS诱导的细胞产生促炎细胞因子（IL-6, ROS和NO），表明其具备显著的抗炎活性。

COX-2 15-LOX-IN-4（compound 5i）是一种针对COX-2和15-LOX的双重抑制剂，其IC50值分别为0.075 μM和1.97 μM。该化合物能有效地阻止LPS诱发的细胞内促炎细胞因子（IL-6, ROS）的产生，表现出明确的抗炎活性。

COX-2 15-LOX-IN-5（Compound 4f）作为一种COX-2 15-LOX双重抑制剂，在脂多糖介导的RAW 264.7巨噬细胞中有效降低NF-κB活化。此外，COX-2 15-LOX-IN-5还表现出显著的抗炎和抗氧化活性。

(S)-Coriolic acid (13(S)-HODE) 是一种重要的细胞内信号剂，是亚油酸与植物和哺乳动物脂氧合酶反应生成的，在各种生物系统中参与细胞增殖和分化。(S)-Coriolic acid 在 1 μM 左右时，它能抑制肿瘤细胞与血管内皮的粘附，能下调 IRGpIIb IIIa 受体的表达。(S)-Coriolic acid 是15-脂氧合酶 (15-LOX) 代谢产物，常作为内源性配体激活 PPARγ。(S)-Coriolic acid 诱导线粒体功能障碍 和气道上皮损伤。

Utreloxastat (PTC857) 是一种新型 15-脂氧合酶抑制剂，可用于研究肌萎缩侧索硬化症 。

ML351 是一种高度特异的15-LOX-1抑制剂，其 IC50=200 nM。它对 T1D 非肥胖糖尿病小鼠模型的血糖异常和β细胞氧化应激有抑制作用。它对相关同工酶 (5-LOX、血小板 12-LOX、15-LOX-2、绵羊 COX-1 和人 COX-2) 表现出良好的选择性(>250倍)。

2-TEDC 是一种有效的脂氧合酶（LOX）抑制剂，对 5-LOX、12-LOX 和 15-LOX 具有抑制作用，IC50 值分别为 0.09 μM、0.013 μM 和 0.5 μM。2-TEDC 可用于研究动脉粥样硬化。

COX-2-IN-26 是有效的、口服具有活力的、选择性的 COX-2 抑制剂，能够作用于 COX-1 (IC50: 10.61 μM)、COX-2 (IC50: 0.067 μM)、15-LOX (IC50: 1.96 μM)。COX-2-IN-26 具有抗炎作用，具有胃肠道安全性。

COX-2-IN-28 是一种有效的、选择性的 COX-2 抑制剂，能够作用于 COX-2 (IC50: 0.054 μM)、15-LOX (IC50: 2.14 μM)、COX-1 (IC50: 13.21 μM)。

ThioLox 是一种竞争性 15-脂氧合酶-1 (15-LOX-1) 抑制剂(IC50值为12 μM)。ThioLox 显示抗炎和神经保护特性。具有抗炎和神经保护作用，对谷氨酸毒性有很强的保护作用。

Caffeoylcalleryanin demonstrated potent inhibitory activity against 15-lipoxygenase (15-LOX), with an IC50 value of 1.59 μM. Furthermore, ethanol extract from A. pulchra leaves (EEAPL) was found to contain compounds exhibiting antiviral properties, particularly effective against Dengue virus type 2 (DENV-2). Among these compounds, Caffeoylcalleryanin emerged as the most potent anti-DENV-2 agent, achieving a selectivity index (SI) of 20.0.

CAY10698 是选择性的12-Lipoxygenase (12-LOX)抑制剂，IC50=5.1 μM。它对 5-LOX、15-LOX-1、15-LOX-2 和 COX-1 2 无活性。

(±)13-HODE cholesteryl ester was originally extracted from atherosclerotic lesions and shown to be produced by Cu2+-catalyzed oxidation of LDL. Later studies determined that 15-LO from rabbit reticulocytes and human monocytes were able to metabolize cholesteryl linoleate, a major component of LDL, to 13-HODE cholesteryl ester.

(±)9-HODE cholesteryl ester was originally extracted from atherosclerotic lesions and shown to be produced by Cu2+-catalyzed oxidation of LDL. Later studies determined that 15-LO from rabbit reticulocytes and human monocytes were able to metabolize cholesteryl linoleate, a major component of LDL, to 9-HODE cholesteryl ester.

(±)14(15)-EET is a metabolite of arachidonic acid that is formed via epoxidation of arachidonic acid by cytochrome P450.[1],[2] It prevents increases in leukotriene B4, ICAM-1, and chemokine (C-C motif) ligand 1 (CCL2) induced by oxidized LDL in primary rat pulmonary artery endothelial cells (RPAECs) when used at a concentration of 1 μM.[3] (±)14(15)-EET induces dilation of preconstricted isolated canine coronary arterioles (EC50 = 0.2 pM).[4] It reduces myocardial infarct size as a percentage of the area at risk in a canine model of ischemia-reperfusion injury induced by left anterior descending coronary artery (LAD) occlusion when administered at a dose of 0.128 mg kg prior to occlusion or reperfusion.[5] Reference：[1]. Chacos, N., Falck, J.R., Wixtrom, C., et al. Novel epoxides formed during the liver cytochrome P-450 oxidation of arachidonic acid. Biochem. Biophys. Res. Commun. 104(3), 916-922 (1982).[2]. Oliw, E.H., Guengerich, F.P., and Oates, J.A. Oxygenation of arachidonic acid by hepatic monooxygenases. Isolation and metabolism of four epoxide intermediates. J. Biol. Chem. 257(7), 3771-3781 (1982).[3]. Jiang, J.-X., Zhang, S.-J., Xiong, Y.-K., et al. EETs attenuate ox-LDL-induced LTB4 production and activity by inhibiting p38 MAPK phosphorylation and 5-LO BLT1 receptor expression in rat pulmonary arterial endothelial cells. PLoS One 10(6), e0128278 (2015).[4]. Oltman, C.L., Weintraub, N.L., VanRollins, M., et al. Epoxyeicosatrienoic acids and dihydroxyeicosatrienoic acids are potent vasodilators in the canine coronary microcirculation. Circ. Res. 83(9), 932-939 (1998).[5]. Nithipatikom, K., Moore, J.M., Isbell, M.A., et al. Epoxyeicosatrienoic acids in cardioprotection: Ischemic versus reperfusion injury. Am. J. Physiol. Heart Circ. Physiol. 291(2), H537-H542 (2006).