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Journal articles on the topic 'COX-2 selective inhibitor'

Author: Grafiati

Published: 7 June 2025

Last updated: 2 August 2025

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1

NAKAMURA, Hideo. "Cyclooxygenase (COX)-2 selective inhibitors: aspirin, a dual COX-1/COX-2 inhibitor, to COX-2 selective inhibitors." Folia Pharmacologica Japonica 118, no. 3 (2001): 219–30. http://dx.doi.org/10.1254/fpj.118.219.

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2

Eibl, Guido, Yasunori Takata, Laszlo G. Boros, et al. "Growth Stimulation of COX-2–Negative Pancreatic Cancer by a Selective COX-2 Inhibitor." Cancer Research 65, no. 3 (2005): 982–90. http://dx.doi.org/10.1158/0008-5472.982.65.3.

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Abstract Cyclooxygenase 2 (COX-2) inhibitors are promising antiangiogenic agents in several preclinical models. The aim of the present study was to evaluate the effect of selective COX-2 inhibitors on vascular endothelial growth factor (VEGF) production in vitro and angiogenesis and growth of pancreatic cancer in vivo, focusing on putative differences between COX-2–negative and COX-2–positive tumors. VEGF production and angiogenesis in vitro were determined by ELISA and endothelial cell migration assay. To determine whether the effect of COX-2 inhibitors was mediated by peroxisome proliferator

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3

&NA;. "Rofecoxib: a selective COX-2 inhibitor." Drugs & Therapy Perspectives 15, no. 2 (2000): 1–5. http://dx.doi.org/10.2165/00042310-200015020-00001.

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4

Martina, Shaunta‘ D., Kimi S. Vesta, and Toni L. Ripley. "Etoricoxib: A Highly Selective COX-2 Inhibitor." Annals of Pharmacotherapy 39, no. 5 (2005): 854–62. http://dx.doi.org/10.1345/aph.1e543.

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OBJECTIVE: To review the available literature evaluating the pharmacology, pharmacokinetics, clinical efficacy, and adverse effects of etoricoxib, a highly selective cyclooxygenase-2 (COX-2) inhibitor that is not currently approved for use in the US. DATA SOURCES: Literature retrieval was accessed through MEDLINE (1966–December 2004), Current Contents (1998–December 2004), and Cochrane Library (4th quarter 2004). References from retrieved articles, information from the manufacturer, and abstracts from the American College of Rheumatology and Annual European Congress of Rheumatology meetings we

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5

Degraeve, Frédéric, Manlio Bolla, Stéphanie Blaie, et al. "Modulation of COX-2 Expression by Statins in Human Aortic Smooth Muscle Cells." Journal of Biological Chemistry 276, no. 50 (2001): 46849–55. http://dx.doi.org/10.1074/jbc.m104197200.

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Cyclooxygenase (COX)-2 and COX-1 play an important role in prostacyclin production in vessels and participate in maintaining vascular homeostasis. Statins are inhibitors of 3-hydroxy-3-methylglutaryl coenzyme A (HMG CoA) reductase, which is crucial in cholesterol biosynthesis. Recently, cholesterol-independent effects of statins have been described. In this study, we evaluated the effect of two inhibitors of HMG CoA reductase, mevastatin and lovastatin, on the production of prostacyclin and the expression of COX in human aortic smooth muscle cells. Treatment of cells with 25 μmmevastatin or lo

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6

Jeger, Raban V., Jeffrey D. Greenberg, Krishnan Ramanathan, and Michael E. Farkouh. "Lumiracoxib, a highly selective COX-2 inhibitor." Expert Review of Clinical Immunology 1, no. 1 (2005): 37–45. http://dx.doi.org/10.1586/1744666x.1.1.37.

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7

&NA;. "Rofecoxib: a selective and effective COX-2 inhibitor." Drugs & Therapy Perspectives 18, no. 2 (2002): 1–3. http://dx.doi.org/10.2165/00042310-200218020-00001.

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8

Miller, Jane L. "Second selective COX-2 inhibitor receives marketing approval." American Journal of Health-System Pharmacy 56, no. 13 (1999): 1294. http://dx.doi.org/10.1093/ajhp/56.13.1294a.

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9

Takahashi, Toshiyuki, and Mitsuo Miyazawa. "N-Caffeoyl serotonin as selective COX-2 inhibitor." Bioorganic & Medicinal Chemistry Letters 22, no. 7 (2012): 2494–96. http://dx.doi.org/10.1016/j.bmcl.2012.02.002.

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10

Zhu, Xi-Tian, Lei Chen, and Jian-Hua Lin. "Selective COX-2 inhibitor versus non-selective COX-2 inhibitor for the prevention of heterotopic ossification after total hip arthroplasty." Medicine 97, no. 31 (2018): e11649. http://dx.doi.org/10.1097/md.0000000000011649.

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11

Saito, Takayuki, Ian W. Rodger, Hani Shennib, Fu Hu, Lara Tayara, and Adel Giaid. "Cyclooxygenase-2 (COX-2) in acute myocardial infarction: cellular expression and use of selective COX-2 inhibitor." Canadian Journal of Physiology and Pharmacology 81, no. 2 (2003): 114–19. http://dx.doi.org/10.1139/y03-023.

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Our previous work has shown strong expression of COX-2 in the myocardium of patients with end-stage ischemic heart failure. The purpose of this study was to determine the cellular expression of this enzyme in the setting of acute myocardial infarction (AMI) and determine the role of COX-2 in experimental animals using a selective COX-2 inhibitor. Experimental AMI was induced in rats by ligating the left coronary artery. Animals were either treated with a selective COX-2 inhibitor (5 mg·kg1·day1) or vehicle. Three days after ligation, cardiac function was assessed and infarct size was determi

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12

Özdemir, Ahmet, and Halide Edip Temel. "COX inhibitory profiles of a series of thiadiazole-benzothiazole hybrids." European Journal of Life Sciences 3, no. 1 (2024): 9–15. http://dx.doi.org/10.55971/ejls.1443664.

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In an endeavour to identify small molecule COX-1 inhibitors, a colorimetric assay protocol was applied for the in vitro evaluation of COX-1 and 2 inhibitory potential of a series of thiadiazole-benzothiazole hybrids. The most potent and selective COX-1 inhibitor in this series was found as 2-[(5-amino-1,3,4-thiadiazol-2-yl)thio]-N-(6-chlorobenzothiazol-2-yl)acetamide (7) (51.36 ± 3.32% at 100 µM) compared to SC-560 (83.64 ± 3.76% at 1 µM). Compound 7 exerted weaker inhibitory effect on COX-2 (11.05 ± 1.69% at 100 µM). To explore its binding interactions at the active site of human COX-1 (PDB I

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13

Ouellet, M., and M. D. Percival. "Effect of inhibitor time-dependency on selectivity towards cyclooxygenase isoforms." Biochemical Journal 306, no. 1 (1995): 247–51. http://dx.doi.org/10.1042/bj3060247.

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Cyclooxygenase (Cox) is a key enzyme in the biosynthesis of prostaglandins and, as such, is the target of non-steroidal anti-inflammatory drugs (NSAIDs). Two isoforms exist, being expressed constitutively (Cox-1), or inducibly in response to inflammatory mediators (Cox-2). Currently available NSAIDs inhibit both isoforms somewhat equipotently but selective Cox-2 inhibition may eliminate unwanted side effects. We have characterized the kinetic mechanisms of the interactions of purified recombinant human cyclooxygenase-1 and -2 (hCox-1, hCox-2) with the selective Cox-2 inhibitor N-(2-cyclohexylo

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14

Gaytán, M., C. Bellido, C. Morales, J. E. Sánchez-Criado, and F. Gaytán. "Effects of selective inhibition of cyclooxygenase and lipooxygenase pathways in follicle rupture and ovulation in the rat." Reproduction 132, no. 4 (2006): 571–77. http://dx.doi.org/10.1530/rep.1.01236.

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Treatment with non-steroidal anti-inflammatory drugs, either non-selective or selective cyclooxygenase-2 (COX-2) inhibitors, consistently impairs ovulation, indicating the essential role of COX-2/prostaglandins in the ovulatory process. Indomethacin, a potent inhibitor of both COX-1 and COX-2, induced several ovulatory alterations, consisting of a decrease in the number of oocytes effectively ovulated, trapping of oocytes inside the luteinized follicle, as well as abnormal follicle rupture at the basolateral sides, with release of the oocyte and follicular fluid to the interstitium. Yet, the p

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15

Hong, Ting-Ting, Jinbao Huang, Terrance D. Barrett, and Benedict R. Lucchesi. "Effects of cyclooxygenase inhibition on canine coronary artery blood flow and thrombosis." American Journal of Physiology-Heart and Circulatory Physiology 294, no. 1 (2008): H145—H155. http://dx.doi.org/10.1152/ajpheart.00646.2007.

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This study was designed to determine the effect of inhibitors of cyclooxygenase (COX)-1, COX-2, and the nonselective COX inhibitor naproxen on coronary vasoactivity and thrombogenicity under baseline and lipopolysaccharide (LPS)-induced inflammatory conditions. We hypothesize that endothelial COX-1 is the primary COX isoform in the canine normal coronary artery, which mediates arachidonic acid (AA)-induced vasodilatation. However, COX-2 can be induced and overexpressed by inflammatory mediators and becomes the major local COX isoform responsible for the production of antithrombotic prostagland

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16

Clyman, Ronald I., Pierre Hardy, Nahid Waleh, et al. "Cyclooxygenase-2 plays a significant role in regulating the tone of the fetal lamb ductus arteriosus." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 276, no. 3 (1999): R913—R921. http://dx.doi.org/10.1152/ajpregu.1999.276.3.r913.

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Nonselective cyclooxygenase (COX) inhibitors are potent tocolytic agents but have adverse effects on the fetal ductus arteriosus. We hypothesized that COX-2 inhibitors may not affect the ductus if the predominant COX isoform is COX-1. To examine this hypothesis, we used ductus arteriosus obtained from late-gestation fetal lambs. In contrast to our hypothesis, fetal lamb ductus arteriosus expressed both COX-1- and COX-2-immunoreactive protein (by Western analysis). Although COX-1 was found in both endothelial and smooth muscle cells, COX-2 was found only in the endothelial cells lining the duct

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17

Charette, L., C. Misquitta, J. Guay, D. Riendeau, and T. R. Jones. "Involvement of cyclooxygenase 2 (COX-2) in intrinsic tone of isolated guinea pig." Canadian Journal of Physiology and Pharmacology 73, no. 11 (1995): 1561–67. http://dx.doi.org/10.1139/y95-215.

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Indomethacin and related nonsteroidal anti-inflammatory drugs relax prostanoid-dependent intrinsic tone of isolated guinea pig trachea by inhibiting cyclooxygenase (COX). Recently, a second isoform of COX (COX-2) was discovered, which differed from COX-1 with respect to protein structure, transcriptional regulation, and susceptibility to inhibition by pharmacological agents. It is now known that indomethacin nonselectively inhibits COX-1 and COX-2, whereas NS-398 is a selective inhibitor of COX-2. In the present study we compared the activity of a selective (NS-398) and nonselective (indometha

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18

Altıntop, Mehlika Dilek, Belgin Sever, Halide Edip Temel, Zafer Asım Kaplancıklı, and Ahmet Özdemir. "Design, Synthesis and In vitro COX Inhibitory Profiles of A New Series of Tetrazole-based Hydrazones." European Journal of Life Sciences 1, no. 1 (2022): 20–27. http://dx.doi.org/10.55971/ejls.1095818.

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Inhibition of cyclooxygenases (COXs), by selective and nonselective inhibitors, is a favorable approach for pharmacologic intervention in a variety of disorders such as cancer. For this purpose, a new class of tetrazole-hydrazone hybrids (1-12) was designed. A facile and efficient procedure was applied for the preparation of compounds 1-12, which were tested for their inhibitory activities towards cyclooxygenases (COXs) by means of an in vitro colorimetric method. The most potent and selective COX-1 inhibitors were determined as 2-[(1-methyl-1H-tetrazol-5-yl)thio]-N'-(4-(piperidin-1-yl)benzyli

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19

Ryan, E. P., I. Rahman, and R. P. Phipps. "Cyclooxygenase-2 inhibition induces oxidative stress and decreases intracellular glutathione to reduce survival of human B lymphoma/leukemia cells." Journal of Clinical Oncology 25, no. 18_suppl (2007): 18522. http://dx.doi.org/10.1200/jco.2007.25.18_suppl.18522.

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18522 We recently reported that inhibition of Cox-2 reduced human B-CLL proliferation and survival. Herein, we investigated the mechanisms whereby a small molecule Cox-2 selective inhibitor (SC-58125) blunts survival of human B cell lymphomas and chronic lymphocytic leukemia B cells. SC-58125 (a celecoxib analogue) and OSU03012 (a celecoxib analogue that lacks Cox-2 inhibitory activity) both decreased intracellular glutathione (GSH) content in malignant human B cells, as well as in Cox-2 deficient mouse B cells. This new finding supports Cox-2 independent effects of SC-58125. Interestingly, SC

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20

Mysler, E. "Lumiracoxib (Prexige®): a new selective cox-2 inhibitor." International Journal of Clinical Practice 58, no. 6 (2004): 606–11. http://dx.doi.org/10.1111/j.1368-5031.2004.00199.x.

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21

&NA;. "Trials supporting selective COX-2 inhibitor safety seriously flawed." Reactions Weekly &NA;, no. 960 (2003): 2. http://dx.doi.org/10.2165/00128415-200309600-00002.

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22

Dickman, Andrew, and John Ellershaw. "For Discussion NSAIDs: gastroprotection or selective COX-2 inhibitor?" Palliative Medicine 18, no. 4 (2004): 275–86. http://dx.doi.org/10.1191/0269216304pm894fd.

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23

Schiffmann, Susanne, Jessica Sandner, Ronald Schmidt, et al. "The selective COX-2 inhibitor celecoxib modulates sphingolipid synthesis." Journal of Lipid Research 50, no. 1 (2008): 32–40. http://dx.doi.org/10.1194/jlr.m800122-jlr200.

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24

Antoniou, Katerina, Michael Malamas, and Alexandros A. Drosos. "Clinical pharmacology of celecoxib, a COX-2 selective inhibitor." Expert Opinion on Pharmacotherapy 8, no. 11 (2007): 1719–32. http://dx.doi.org/10.1517/14656566.8.11.1719.

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25

Dallob, Aimee, Christopher J. Hawkey, Howard Greenberg, et al. "Characterization of Etoricoxib, a Novel, Selective COX-2 Inhibitor." Journal of Clinical Pharmacology 43, no. 6 (2003): 573–85. http://dx.doi.org/10.1177/0091270003253703.

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26

Whitehead, Andrew J., Richard A. Ward, and Martin F. Jones. "Efficient synthesis of the selective COX-2 inhibitor GW406381X." Tetrahedron Letters 48, no. 6 (2007): 911–13. http://dx.doi.org/10.1016/j.tetlet.2006.12.045.

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27

Jones, Richard A. "Etodolac: An overview of a selective COX-2 inhibitor." Inflammopharmacology 7, no. 3 (1999): 269–75. http://dx.doi.org/10.1007/s10787-999-0010-3.

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28

Miyamoto, K. "Selective COX-2 inhibitor celecoxib prevents experimental autoimmune encephalomyelitis through COX-2-independent pathway." Brain 129, no. 8 (2006): 1984–92. http://dx.doi.org/10.1093/brain/awl170.

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29

Watson, Douglas J., Sean E. Harper, Peng-Liang Zhao, Hui Quan, James A. Bolognese, and Thomas J. Simon. "Gastrointestinal Tolerability of the Selective Cyclooxygenase-2 (COX-2) Inhibitor Rofecoxib Compared With Nonselective COX-1 and COX-2 Inhibitors in Osteoarthritis." Archives of Internal Medicine 160, no. 19 (2000): 2998. http://dx.doi.org/10.1001/archinte.160.19.2998.

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30

Sharma, Rajesh, Jitendra Sainy, and Subhash Chaturvedi. "2-Amino-5-sulfanyl-1,3,4-thiadiazoles: A new series of selective cyclooxygenase-2 inhibitors." Acta Pharmaceutica 58, no. 3 (2008): 317–26. http://dx.doi.org/10.2478/v10007-008-0011-6.

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2-Amino-5-sulfanyl-1,3,4-thiadiazoles: A new series of selective cyclooxygenase-2 inhibitorsA new series of cyclooxygenase-2 inhibitors with 2-amino--5-sulfanyl-1,3,4-thiadiazole as the central scaffold unit has been synthesized. The newly synthesized compounds were characterized by analytical and spectral methods. Compounds were screened for cyclooxygenase inhibitory activity by the colorimetric COX (ovine) inhibitor screening assay, anti-inflammatory activity by the carrageenean induced rat paw oedema test and analgesic activity by the tail flick method. Some compounds exhibited significant

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31

Gurgel, Bruno César de Vasconcelos, Fernanda Vieira Ribeiro, Marco Antônio Dias da Silva, et al. "Selective COX-2 inhibitor reduces bone healing in bone defects." Brazilian Oral Research 19, no. 4 (2005): 312–16. http://dx.doi.org/10.1590/s1806-83242005000400014.

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Anti-inflammatory agents have been reported to regulate bone healing. The aim of this study was to investigate the effect of a selective cyclooxygenase-2 inhibitor (meloxicam) on bone healing in calvarial defects in rats. Thirty-six adult male Wistar rats were included. After anesthesia, a linear incision was made through the skin of the scalp, a full-thickness flap was reflected and a 4 mm round defect was made with a trephine drill. The animals were randomly assigned to one of the following 4 treatment groups (9 animals each), including daily subcutaneous injections: A: saline solution for 1

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32

Schlemper, Valfredo, and João B. Calixto. "Mechanisms underlying the contraction induced by bradykinin in the guinea pig epithelium-denuded trachea." Canadian Journal of Physiology and Pharmacology 80, no. 4 (2002): 360–67. http://dx.doi.org/10.1139/y02-061.

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This study investigates some of the mechanisms by which bradykinin (BK) triggers contraction of epithelium-denuded strips of guinea pig trachea (GPT). Cumulative or single additions of BK, T-BK, L-BK, or ML-BK in the presence of captopril (30 µM) produced graded GPT contractions with the following rank order of potency (EC50 level): T-BK (31.3 nM) > BK (40.0 nM) > L-BK (56.0 nM) > ML-BK (77.0 nM). BK-induced contraction (100 nM) in GPT was completely inhibited by either HOE 140 or NPC 17731 with mean IC50 values of 17 and 217 nM, respectively. Addition of BK (100 nM) at 30 min interva

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33

Menozzi, Alessandro, Cristina Pozzoli, Enzo Poli, Lucia Tagliaferri, Giuseppe Placenza, and Simone Bertini. "Effects of nonselective and selective cyclooxygenase inhibitors on the contractions of isolated bronchial smooth muscle in the horse." Acta Veterinaria Brno 87, no. 2 (2018): 99–107. http://dx.doi.org/10.2754/avb201887020099.

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We evaluated the effects of nonselective cyclooxygenase (COX)-1/COX-2 inhibitors (acetylsalicylic acid, indomethacin, ibuprofen, flunixin meglumine, phenylbutazone), preferential COX-2 inhibitors (diclofenac, meloxicam, carprofen), selective COX-1 inhibitor (SC-560), and selective COX-2 inhibitors (celecoxib, firocoxib, parecoxib) on the contractions of isolated bronchi induced by electrical field stimulation (EFS). Bronchial rings, obtained from lungs of slaughtered horses, were put in isolated organ baths, and the mechanical activity was measured by means of isotonic transducers. Electrical

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34

Kim, Min Ji, Hwi-Ho Lee, Choi Kim, et al. "Selective mPGES-1 Inhibitor Ameliorated Adjuvant-Induced Arthritis in the Rat Model." Journal of Chemistry 2024 (February 13, 2024): 1–8. http://dx.doi.org/10.1155/2024/5531519.

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Endogenous prostaglandin E2 (PGE2) plays an important role in maintaining the homeostasis conditions. However, the overexpression of PGE2 in response to various inflammatory stimulations is an important target of anti-inflammatory drugs. Both inducible COX-2 (cyclooxygenase-2) and mPGES-1 (microsomal prostaglandin E2 synthase-1) enzymes are responsible for the inflammatory overexpressed PGE2 production. Among them, mPGES-1 is regarded as a more promising ideal target for anti-inflammatory drugs without the gastrointestinal and cardiovascular side effects. As our continuous research for the dis

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35

Yamamoto, Tatsuo, and Natsuko Nozaki-Taguchi. "Analysis of the effects of cyclooxygenase (COX)-1 and COX-2 in spinal nociceptive transmission using indomethacin, a non-selective COX inhibitor, and NS-398, a COX-2 selective inhibitor." Brain Research 739, no. 1-2 (1996): 104–10. http://dx.doi.org/10.1016/s0006-8993(96)00817-7.

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36

Patrignani, Paola, Marta L. Capone, and Stefania Tacconelli. "Clinical pharmacology of etoricoxib: a novel selective COX-2 inhibitor." Expert Opinion on Pharmacotherapy 4, no. 2 (2003): 265–84. http://dx.doi.org/10.1517/eoph.4.2.265.21085.

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37

Tian, Feng, Lin Wang, and Ya-Jie Zhang. "Selective COX-2 inhibitor celecoxib inhibits liver fibrogenesis in rats." World Chinese Journal of Digestology 19, no. 19 (2011): 2002. http://dx.doi.org/10.11569/wcjd.v19.i19.2002.

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38

Grobelny, Pawel, Arijit Mukherjee, and Gautam R. Desiraju. "Polymorphs and hydrates of Etoricoxib, a selective COX-2 inhibitor." CrystEngComm 14, no. 18 (2012): 5785. http://dx.doi.org/10.1039/c2ce06604a.

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39

Myoung, Hoon. "Anti-Cancer Effects of a Selective Cox-2 Inhibitor, Celecoxib." Journal of Oral and Maxillofacial Surgery 65, no. 9 (2007): 35.e3–35.e4. http://dx.doi.org/10.1016/j.joms.2007.06.608.

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40

Schattenkirchner, Manfred. "Meloxicam:a selective COX-2 inhibitor non-steroidal anti-inflammatory drug." Expert Opinion on Investigational Drugs 6, no. 3 (1997): 321–34. http://dx.doi.org/10.1517/13543784.6.3.321.

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41

TALHARI, C., I. LAUCEVICIUTE, E. ENDERLEIN, T. RUZICKA, and B. HOMEY. "COX-2–selective inhibitor valdecoxib induces severe allergic skin reactions." Journal of Allergy and Clinical Immunology 115, no. 5 (2005): 1089–90. http://dx.doi.org/10.1016/j.jaci.2004.12.1135.

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42

Xu, Xiangbo, Xihua Chen, Yunfeng Li та ін. "Cyclooxygenase-2 Regulated by the Nuclear Factor-κB Pathway Plays an Important Role in Endometrial Breakdown in a Female Mouse Menstrual-like Model". Endocrinology 154, № 8 (2013): 2900–2911. http://dx.doi.org/10.1210/en.2012-1993.

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Abstract The role of prostaglandins (PGs) in menstruation has long been proposed. Although evidence from studies on human and nonhuman primates supports the involvement of PGs in menstruation, whether PGs play an obligatory role in the process remains unclear. Although cyclooxygenase (COX) inhibitors have been used in the treatment of irregular uterine bleeding, the mechanism involved has not been elucidated. In this study, we used a recently established mouse menstrual-like model for investigating the role of COX in endometrial breakdown and its regulation. Administration of the nonspecific C

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43

EL-Shazly, Amany, Amal EL-Gohary, Laila EL-Shazly, and Ghada EL-Hossary. "Comparison between two cyclooxygenase inhibitors in an experimental dry eye model in albino rabbits." Acta Pharmaceutica 58, no. 2 (2008): 163–73. http://dx.doi.org/10.2478/v10007-008-0009-0.

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Comparison between two cyclooxygenase inhibitors in an experimental dry eye model in albino rabbitsThe purpose of this study was to compare the topical anti-inflammatory effects of the nonselective cyclooxygenase (COX) inhibitor, ketorolac, with the selective COX-2 inhibitor, nimesulide, in an animal model of dry eye in albino rabbits. All animals were examined by the Schirmer test, tear break-up time (TBUT) and fluorescein corneal staining test. Dry eye model showed significant reduction in tear volume, TBUT, corneal staining and histopathological signs of dryness and inflammation. On treatin

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44

Assali, Mohyeddin, Murad Abualhasan, Hadeel Sawaftah, Mohammed Hawash, and Ahmed Mousa. "Synthesis, Biological Activity, and Molecular Modeling Studies of Pyrazole and Triazole Derivatives as Selective COX-2 Inhibitors." Journal of Chemistry 2020 (March 24, 2020): 1–14. http://dx.doi.org/10.1155/2020/6393428.

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Series of diaryl-based pyrazole and triazole derivatives were designed and synthesized in a facile synthetic approach in order to produce selective COX-2 inhibitor. These series of derivatives were synthesized by different reactions like Vilsmeier–Haack reaction and click reaction. In vitro COX-1 and COX-2 inhibition studies showed that five compounds were potent and selective inhibitors of the COX-2 isozyme with IC50 values in 0.551–0.002 μM range. In the diarylpyrazole derivatives, compound 4b showed the best inhibitory activity against COX-2 with IC50 = 0.017 μM as one of the N-aromatic rin

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45

Farzaneh, Shabnam, Elnaz Zeinalzadeh, Bahram Daraei, Soraya Shahhosseini, and Afshin Zarghi. "New Ferrocene Compounds as Selective Cyclooxygenase (COX-2) Inhibitors: Design, Synthesis, Cytotoxicity and Enzyme-inhibitory Activity." Anti-Cancer Agents in Medicinal Chemistry 18, no. 2 (2018): 295–301. http://dx.doi.org/10.2174/1871520617666171003145533.

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Background: Due to the astonishing properties of ferrocene and its derivatives, it has a broad application in diverse areas. Numerous ferrocene derivatives demonstrated anti-proliferative activity. Also COX-2, as a key isoenzyme for production of prostaglandins, is frequently overexpressed in various cancers. It is now recognized that COX-2 over expression promotes tumorigenic functions which can be suppressed by COX-2 inhibitors, a phenomenon useful for the preventing of tumor progression. The combination of COX-2 inhibitors with other anti-cancer or cancer prevention drugs may reduce their s

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46

Black, W. C., C. Bayly, M. Belley, et al. "From indomethacin to a selective COX-2 inhibitor: Development of indolalkanoic acids as potent and selective cyclooxygenase-2 inhibitors." Bioorganic & Medicinal Chemistry Letters 6, no. 6 (1996): 725–30. http://dx.doi.org/10.1016/0960-894x(96)00100-x.

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Gariepy, Helaine, Jun Zhao, and Dan Levy. "Differential contribution of COX-1 and COX-2 derived prostanoids to cortical spreading depression—Evoked cerebral oligemia." Journal of Cerebral Blood Flow & Metabolism 37, no. 3 (2016): 1060–68. http://dx.doi.org/10.1177/0271678x16650217.

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Cortical spreading depression (CSD) is considered a significant phenomenon for human neurological conditions and one of its key signatures is the development of persistent cortical oligemia. The factors underlying this reduction in cerebral blood flow (CBF) remain incompletely understood but may involve locally elaborated vasoconstricting eicosanoids. We employed laser Doppler flowmetry in urethane-anesthetized rats, together with a local pharmacological blockade approach, to test the relative contribution of cyclooxygenase (COX)-derived prostanoids to the oligemic response following CSD. Admi

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Haq, Kautsar Ul, Nur Lailatus Sa'adah, Imam Siswanto, and Hery Suwito. "Bioactivity of dihydropyrimidinone derivatives as inhibitors of cyclooxygenase-2 (COX-2): an in silico approach." RSC Advances 13, no. 49 (2023): 34348–57. http://dx.doi.org/10.1039/d3ra05942a.

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Longo, Walter E., Brian Erickson, Ninder Panesar, John E. Mazuski, Sandra Robinson, and Donald L. Kaminski. "The role of selective cyclooxygenase isoforms in human intestinal smooth muscle cell stimulated prostanoid formation and proliferation." Mediators of Inflammation 7, no. 6 (1998): 373–80. http://dx.doi.org/10.1080/09629359890749.

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Intestinal smooth muscle plays a major role in the repair of injured intestine and contributes to the prostanoid pool during intestinal inflammatory states. Cyclooxygenase (COX), which catalyzes the conversion of arachidonic acid to prostanoids exists in two isoforms, COX-1 and COX-2. The purpose of this study was to determine the relative contributions of COX-1 and COX-2 in the production of prostanoids by human intestinal smooth muscle (HISM) cells when stimulated by interleukin-1β (IL-1β) and lipopolsaccharide (LPS). Furthermore the effects of specific COX-1 and COX-2 inhibitors on the prol

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Miladiyah, Isnatin, Jumina Jumina, Sofia Mubarika Haryana, and Mustofa Mustofa. "IN SILICO MOLECULAR DOCKING OF XANTHONE DERIVATIVES AS CYCLOOXYGENASE-2 INHIBITOR AGENTS." International Journal of Pharmacy and Pharmaceutical Sciences 9, no. 3 (2017): 98. http://dx.doi.org/10.22159/ijpps.2017v9i3.15382.

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Objective: To demonstrate the potential ofdifferent xanthone derivatives as cyclooxygenase-2 (COX-2) inhibitor agents and their selectivity against cycloooxygenase-1 (COX-1) and COX-2 using molecular simulation.Methods: Nine novel xanthone derivatives (compounds A-I) were employed to dock against protein COX-2 (Protein Data Bank/PDB ID: 1CX2) and COX-1 (PDB ID: 3N8Z). Celecoxib, a selective COX-2 inhibitor, was chosen as a control compound. The free binding energy produced by the docking was scored using Protein-Ligand Ant System (PLANTS) and the hydrogen bonds (H-bonds) between ligands and en

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