myeloperoxidase

4-POBN (Myeloperoxidase Inhibitor 1) 是一种有效且不可逆的髓过氧化物酶抑制剂 (IC50 = 0.3 µM)。 4-POBN 可用于亚急性中风的研究。

Verdiperstat (AZD 3241) 是一种不可逆的、选择性的、口服具有活力的髓过氧化物酶 (myeloperoxidase) 抑制剂，IC50=630 nM，可用于研究大脑神经退行性疾病。

Anti-Mouse myeloperoxidase MPO Antibody (6D1) 为针对MPO的小鼠来源IgG2bkappa 抗体。其同型对照为 MouseIgG2bkappa, Isotype Control。

Anti-Mouse myeloperoxidase MPO Antibody (6G4) 是一种来自小鼠的IgG2c, κ型抗体抑制剂，用于抗小鼠myeloperoxidase MPO。

PF06282999 是选择性的髓过氧物酶 (myeloperoxidase) 抑制剂，用于研究心血管疾病。

Mitiperstat 是一种强效的骨髓过氧化物酶（MPO）抑制剂。Mitiperstat 对预防如心力衰竭和冠状动脉疾病类的心血管疾病有很好的效果。

MPO-IN-1 是一种具有口服活性的髓过氧化物酶 (MPO) 抑制剂，抑制 MPO 和甲状腺过氧化物 (TPO)，可用于研究炎症。

3-Chloro-L-Tyrosine (Chlorotyrosine) 是一种髓过氧化物酶催化氧化的特异性标志物，在从人动脉粥样硬化内膜分离的低密度脂蛋白中显著升高。

4-Methylesculetin (Methylesculetin) 是口服具有活力的天然香豆素衍生物，有抗氧化、抗炎特性。它可抑制myeloperoxidase 的特性，抑制 IL-6 的水平

Avacopan (CCX168) 是一种 C5aR 拮抗剂 (IC50=0.1 nM)，具有选择性和口服活性。Avacopan 可阻断 C5a 的作用并防止 AAV 小鼠模型中抗髓过氧化物酶抗体诱导的 GN 发展。Avacopan 可以用于治疗抗中性粒细胞胞浆抗体 (ANCA) 相关血管炎。

AZD5904 是一种不可逆的人髓过氧化物酶选择性抑制剂，其IC50=140 nM，在小鼠和大鼠中也具有相似的效力。

MPO-IN-8 是一种口服活性髓过氧化物酶 (MPO) 抑制剂，能够抑制中性粒细胞产生次氯酸和胞外陷阱释放 (NETosis)。在痛风性关节炎模型的小鼠中，该化合物可以有效减轻水肿，降低过氧化物酶活性及IL-1β水平。

10-Methoxy-canthin-6-one (Mtx-C) 作为一种有效的DNA损伤诱导剂，主要通过嵌入DNA促使细胞周期在G2 M期停滞。这一机制有助于诱导急性髓性白血病细胞 (AML) 以及白血病干细胞 (LSC) 的髓系分化。在AML和LSC细胞中，髓系分化主要通过髓过氧化物酶、CD15、CD11b及CD14的表达增强以及p38 MAPK的激活来体现。因此，10-Methoxy-canthin-6-one 在白血病研究领域具有重要应用价值。

9(10)-Nitrooleate，一个内源性脂质信号分子混合体，主要由9-硝基油酸和10-硝基油酸组成。在过氧亚硝酸、酸化亚硝酸和髓过氧化物酶的作用下，该化合物通过与过氧化氢（H2O2）和亚硝酸反应，硝化油酸而形成。

X-17 是一种强效的Vanin-1抑制剂，具有显著的抗炎和抗氧化活性。它能够抑制炎症因子的表达和髓过氧化物酶的活性，同时提高结肠中的谷胱甘肽储备，并恢复肠道屏障功能。

AB8939 是一种高效的小分子微管蛋白 (Microtubule Tubulin) 聚合抑制剂，具有抗肿瘤活性 (抑制肿瘤细胞增殖IC50≤10 nM)。它能够有效规避由 P-糖蛋白和髓过氧化物酶介导的耐药机制，并可诱导细胞在 G2 M 期发生细胞周期停滞和细胞凋亡。

HX1 is a potent reversible myeloperoxidase (MPO) inhibitor.

Resolvin E2 (RvE2) is a member of the specialized pro-resolving mediator (SPM) family of bioactive lipids.1It is produced from eicosapentaenoic acidviaan 18-HEPE intermediate, which is formed by aspirin-acetylated COX-2-mediated oxidation of EPA, by 5-lipoxygenase (5-LO) in human polymorphonuclear (PMN) neutrophils.2,3RvE2 (20 ng/animal) inhibits increases in inflammatory exudate neutrophil infiltration in a mouse model of peritonitis induced by zymosan A .3Hepatic RvE2 levels are increased in mice fed normal chow, as well as in a mouse model of high-fat diet-induced non-alcoholic fatty liver disease (NAFLD), by dietary supplementation with EPA.4Plasma levels of RvE2 are increased by dietary supplementation with fish oil containing ω-3 polyunsaturated fatty acids (PUFAs) in patients with peripheral artery disease or chronic kidney disease.1,5,6 1.Chiang, N., and Serhan, C.N.Specialized pro-resolving mediator network: An update on production and actionsEssays Biochem.64(3)443-462(2020) 2.Tjonahen, E., Oh, S.F., Siegelman, J., et al.Resolvin E2: Identification and anti-inflammatory actions: Pivotal role of human 5-lipoxygenase in resolvin E series biosynthesisChemistry & Biology131193-1202(2006) 3.Sungwhan, F.O., Pillai, P.S., Recchiuti, A., et al.Pro-resolving actions and stereoselective biosynthesis of 18S E-series resolvins in human leukocytes and murine inflammationJ. Clin. Invest.121(2)569-581(2011) 4.Echeverría, F., Valenzuela, R., Espinosa, A., et al.Reduction of high-fat diet-induced liver proinflammatory state by eicosapentaenoic acid plus hydroxytyrosol supplementation: Involvement of resolvins RvE1/2 and RvD1/2J. Nutr. Biochem.6335-43(2019) 5.Ramirez, J.L., Gasper, W.J., Khetani, S.A., et al.Fish oil increases specialized pro-resolving lipid mediators in PAD (the OMEGA-PAD II trial)J. Surg. Res.238164-174(2019) 6.Barden, A.E., Shinde, S., Burke, V., et al.The effect of n-3 fatty acids and coenzyme Q10 supplementation on neutrophil leukotrienes, mediators of inflammation resolution and myeloperoxidase in chronic kidney diseaseProstaglandins Other Lipid Mediat.1361-8(2018)

2-chloro Palmitic acid is a monochlorinated form of palmitic acid . It is produced in a myeloperoxidase (MPO) and time-dependent manner in neutrophils stimulated by phorbol 12-myristate 13-acetate . 2-chloro Palmitic acid (10 μM) induces neutrophil extracellular trap (NET) formation (NETosis) in human neutrophils, increasing DNA release from neutrophils, colocalization of MPO with extracellular DNA (ecDNA), and trapping of E. coli. It increases COX-2 protein levels in human coronary artery endothelial cells (HCAECs) when used at a concentration of 50 μM and increases production of P-selectin, von Willebrand factor, and angiopoietin-2 in HCAECs, as well as neutrophil and platelet adherence, when used at a concentration of 10 μM. 2-chloro Palmitic acid (10-50 μM) also induces apoptosis in THP-1 cells and primary human monocytes and increases caspase-3 activity in THP-1 cells.

5-Chlorouracil is a chlorinated derivative of the pyrimidine nucleoside base uracil . In vivo, it is converted into chlorodeoxyuridine, which is mutagenic and genotoxic.1 Uracil is chlorinated at the 5 position in a cell-free myeloperoxidase, peroxide, and chloride system in which hypochlorous acid is formed.2 5-Chlorouracil has been found in human neutrophils stimulated with phorbol 12-myristate 13-acetate in vitro and in inflammatory human exudate isolated from sites of superficial infection. Levels of 5-chlorouracil are increased in exudate isolated from the site of inflammation in a rat model of carrageenan-induced inflammation and in patient-derived human atherosclerotic aortic tissue.3,4References 5-Chlorouracil is a chlorinated derivative of the pyrimidine nucleoside base uracil . In vivo, it is converted into chlorodeoxyuridine, which is mutagenic and genotoxic.1 Uracil is chlorinated at the 5 position in a cell-free myeloperoxidase, peroxide, and chloride system in which hypochlorous acid is formed.2 5-Chlorouracil has been found in human neutrophils stimulated with phorbol 12-myristate 13-acetate in vitro and in inflammatory human exudate isolated from sites of superficial infection. Levels of 5-chlorouracil are increased in exudate isolated from the site of inflammation in a rat model of carrageenan-induced inflammation and in patient-derived human atherosclerotic aortic tissue.3,4 References

O-Desmethyl-N-deschlorobenzoyl indomethacin is a metabolite of the non-steroidal anti-inflammatory drug (NSAID) and COX inhibitor indomethacin .1It is formed from indomethacin in isolated rabbit hepatocytes. O-Desmethyl-N-deschlorobenzoyl indomethacin (600 μM) decreases the viability of HL-60 leukemia cells when cultured with glucose oxidase.2It has also been used in the synthesis of prostaglandin D2receptor antagonists.3 1.Evans, M.A., Papazafiratou, C., Bhat, R., et al.Indomethacin metabolism in isolated neonatal and fetal rabbit hepatocytesPediatr. Res.15(11)1406-1410(1981) 2.Morgan, A.G.M., Babu, D., Michail, K., et al.An evaluation of myeloperoxidase-mediated bio-activation of NSAIDs in promyelocytic leukemia (HL-60) cells for potential cytotoxic selectivityToxicol. Lett.28048-56(2017) 3.Torisu, K., Kobayashi, K., Iwahashi, M., et al.Discovery of new chemical leads for prostaglandin D2 receptor antagonistsBioorg. Med. Chem. Lett.14(17)4557-4562(2004)

Olsalazine-13C6is intended for use as an internal standard for the quantification of olsalazine by GC- or LC-MS. Olsalazine is an orally bioavailable prodrug form of the anti-inflammatory agent 5-aminosalicylic acid that is cleaved by bacterial azo reductases in the gut to generate active 5-ASA.1In vitro, olsalazine increases ion transport in isolated rabbit distal ileum when applied to the luminal side (ED50= 0.3 mM) and stimulates fluid transport in rat jejunum when used at a concentration of 5 mM.2,3Olsalazine (150 mg/kg for 8 days) improves stool consistency and decreases occult and gross bleeding as well as myeloperoxidase (MPO) activity and leukotriene B4levels in colon tissue in a mouse model of acute colitis induced by dextran sulfate .4Olsalazine also inhibits bovine xanthine oxidasein vitro(IC50= 3.4 mg/L) and lowers serum uric acid levels in a mouse model of hyperuricemia induced by oxonic acid when administered at a dose of 20 mg/kg.5Formulations containing olsalazine have been used in the treatment of inflammatory bowel disease (IBD) and ulcerative colitis. 1.Nugent, S.G., Kumar, D., Rampton, D.S., et al.Intestinal luminal pH in inflammatory bowel disease: Possible determinants and implications for therapy with aminosalicylates and other drugsGut48(4)571-577(2001) 2.Pamukcu, R., Hanauer, S.B., and Chang, E.B.Effect of disodium azodisalicylate on electrolyte transport in rabbit ileum and colon in vitro. Comparison with sulfasalazine and 5-aminosalicylic acidGastroenterology95(4)975-981(1988) 3.Mohsen, A.Q.M., Mulvey, D., Priddle, J.D., et al.Effects of olsalazine in the jejunum of the ratGut28(3)346-352(1987) 4.Murthy, S., Murthy, N.S., Coppola, D., et al.The efficacy of BAY y 1015 in dextran sulfate model of mouse colitisInflamm. Res.46(6)224-233(1997) 5.Niu, Y., Li, H., Gao, L., et al.Old drug, new indication: Olsalazine sodium reduced serum uric acid levels in mice via inhibiting xanthine oxidoreductase activityJ. Pharmacol. Sci.135(3)114-120(2017)

Nitrated unsaturated fatty acids, such as 10- and 12-nitrolinoleate , cholesteryl nitrolinoleate, and nitrohydroxylinoleate, represent a new class of endogenous lipid-derived signalling molecules. LNO2 isomers serve as potent endogenous ligands for PPARγ and can also decompose or be metabolized to release nitric oxide. 9-Nitrooleate is one of two regioisomers of nitrooleate, the other being 10-nitrooleate (OA-NO2; used for the mixture of isomers), which are formed by nitration of oleic acid in approximately equal proportions in vivo. Peroxynitrite, acidified nitrite, and myeloperoxidase in the presence of H2O2 and nitrite, all mediate the nitration of oleic acid. OA-NO2 is found in human plasma as the free acid and esterified in phospholipids at concentrations of 619 ± 52 nM and 302 ± 369 nM, respectively. OA-NO2 activates PPARγ approximately 7-fold at a concentration of 1 μM and effectively promotes differentiation 3T3-L1 preadipocytes to adipocytes at 3 μM.

9(E),11(E)-12-nitro Conjugated linoleic acid (9(E),11(E)-12-nitro CLA) is a nitrated fatty acid. It is formed from 9(Z),11(E)-CLA upon exposure to acidified nitrite, peroxynitrite, gaseous nitrogen dioxide, or a combination of myeloperoxidase, hydrogen peroxide, and nitrite.1It is also formed in LPS-stimulated RAW 264.7 macrophages, an effect that can be reduced by the nitric oxide synthase (NOS) inhibitor L-NAME .29(E),11(E)-12-nitro CLA has been found in human plasma. 1.Woodcock, S.R., Salvatore, S.R., Bonacci, G., et al.Biomimetic nitration of conjugated linoleic acid: Formation and characterization of naturally occurring conjugated nitrodienesJ. Org. Chem.79(1)25-33(2014) 2.Bonacci, G., Baker, P.R.S., Salvatore, S.R., et al.Conjugated linoleic acid is a preferential substrate for fatty acid nitrationJ. Biol. Chem.287(53)44071-44082(2012)