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1

Rubin, Bernard R. "Specific cyclooxygenase-2 (COX-2) inhibitors." Journal of the American Osteopathic Association 99, no. 6 (1999): 322. http://dx.doi.org/10.7556/jaoa.1999.99.6.322.

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2

Reitz, David B., and Peter C. Isakson. "Cyclooxygenase-2 Inhibitors." Current Pharmaceutical Design 1, no. 2 (1995): 211–20. http://dx.doi.org/10.2174/1381612801666220917221427.

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Prostaglandins are synthesized by the enzyme cyclooxygenase (COX), which is the target for nonsteroidal anti-inflammatory drugs (NSAIDs). Recently a second form of COX was discovered (COX-2) that is induced by inflammatory stimuli. The identification of an inducible form of COX led to the hypothesis that COX-2 is responsible for inflammatory prostaglandins, whereas the constitutive COX-I produces physiologically important prostaglandins, e.g., in stomach and kidney. Selective COX- 2 inhibitors have been shown to be anti-inflammatory but do not cause ulcers in the stomach or intestines. It is a
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3

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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4

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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5

Milas, Luka. "Cyclooxygenase-2 (COX-2) Enzyme Inhibitors and Radiotherapy." American Journal of Clinical Oncology 26, Supplement 2 (2003): S66—S69. http://dx.doi.org/10.1097/01.coc.0000074160.49879.51.

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6

Talley, John J., Stephen R. Bertenshaw, David L. Brown, et al. "4,5-Diaryloxazole inhibitors of cyclooxygenase-2 (COX-2)." Medicinal Research Reviews 19, no. 3 (1999): 199–208. http://dx.doi.org/10.1002/(sici)1098-1128(199905)19:3<199::aid-med1>3.0.co;2-7.

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7

Grösch, Sabine, Thorsten Jürgen Maier, Susanne Schiffmann, and Gerd Geisslinger. "Cyclooxygenase-2 (COX-2)–Independent Anticarcinogenic Effects of Selective COX-2 Inhibitors." JNCI: Journal of the National Cancer Institute 98, no. 11 (2006): 736–47. http://dx.doi.org/10.1093/jnci/djj206.

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8

Mengle-Gaw, Laurel J., and Benjamin D. Schwartz. "Cyclooxygenase-2 inhibitors: promise or peril?" Mediators of Inflammation 11, no. 5 (2002): 275–86. http://dx.doi.org/10.1080/09629350290000041.

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The discovery of two isoforms of the cyclooxygenase enzyme, COX-1 and COX-2, and the development of COX-2-specific inhibitors as anti-inflammatories and analgesics have offered great promise that the therapeutic benefits of NSAIDs could be optimized through inhibition of COX-2, while minimizing their adverse side effect profile associated with inhibition of COX-1. While COX-2 specific inhibitors have proven to be efficacious in a variety of inflammatory conditions, exposure of large numbers of patients to these drugs in postmarketing studies have uncovered potential safety concerns that raise
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9

Ray, Neelanjana, Margaret E. Bisher, and L. W. Enquist. "Cyclooxygenase-1 and -2 Are Required for Production of Infectious Pseudorabies Virus." Journal of Virology 78, no. 23 (2004): 12964–74. http://dx.doi.org/10.1128/jvi.78.23.12964-12974.2004.

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ABSTRACT We have recently shown that cyclooxygenase-2 (COX-2) transcription is markedly induced after herpes simplex virus type 1 and pseudorabies virus (PRV) infections of rat embryonic fibroblast (REF) cells (N. Ray and L. W. Enquist, J. Virol. 78:3489-3501, 2004). For this study, we investigated the role of cyclooxygenase induction in the replication and growth of PRV. We demonstrate here a concordant increase in COX-2 mRNA and protein levels after the infection of REF cells. Inhibitors blocking the activity of cyclooxygenases caused a dramatic reduction in PRV growth. Viral growth could be
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10

Pavan, Prabhakar Chinchole, Suresh Adhao Vaibhav, Suresh Adhao Vaibhav, Devidas Mehetre Gautam, Ramesh Thenge Raju, and Ramesh Popat Ritesh. "In Silico study of 3-D structural interactions and quantitative structural drug likeness of marketed Cox-2 inhibitors." GSC Biological and Pharmaceutical Sciences 19, no. 1 (2022): 149–53. https://doi.org/10.5281/zenodo.6624284.

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In the field of molecular modeling, docking may be a method which predicts the well-liked orientation of any molecule to a receptor to make a stable complex. Knowledge of the well-liked orientation successively could also be able to predict the strength of association or binding affinity between two molecules using, for instance, scoring functions. Cyclooxygenase-2 (COX-2) inhibitors block cyclooxygenase-2 (COX-2), an enzyme that promotes inflammation. COX-2 enzyme converts to prostaglandin via arachidonic acid, causing pain and inflammatory responses. They are mainly present in places of infl
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11

Hofer, Michal, and Milan Pospíšil. "Stimulated recovery of perturbed haematopoiesis by inhibition of prostaglandin production — promising therapeutic strategy." Open Life Sciences 1, no. 4 (2006): 584–93. http://dx.doi.org/10.2478/s11535-006-0033-3.

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AbstractInhibitors of prostaglandin production, designated as classical non-steroidal anti-inflammatory drugs (NSAIDs) and acting on the base of non-selective inhibition of cyclooxygenases, have been found in numerous studies to potentiate recovery of perturbed haematopoiesis by removing the negative feedback control mediated by prostaglandins. However, classical NSAIDs show pronounced undesirable gastrointestinal side effects, which limits the possibility of their utilization for various pathophysiological states including myelosuppression. Specific cyclooxygenase-2 (COX-2) inhibitors, target
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12

Ashok, Varun, Chiranjeev Dash, Thomas E. Rohan, J. Michael Sprafka, and Paul D. Terry. "Selective cyclooxygenase-2 (COX-2) inhibitors and breast cancer risk." Breast 20, no. 1 (2011): 66–70. http://dx.doi.org/10.1016/j.breast.2010.07.004.

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13

Talley, John J., and et al et al. "ChemInform Abstract: 4,5-Diaryloxazole Inhibitors of Cyclooxygenase-2 (COX-2)." ChemInform 30, no. 29 (2010): no. http://dx.doi.org/10.1002/chin.199929286.

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14

Lilly, Michael B., Leslie Drapiza, Milan Sheth, Marina Zemskova, Svetlana Bashkirova, and Joan Morris. "Expression of Cyclooxygenase-2 (COX-2) in Human Leukemias and Hematopoietic Cells." Blood 104, no. 11 (2004): 4336. http://dx.doi.org/10.1182/blood.v104.11.4336.4336.

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Abstract COX-2 has been implicated in the development of many epithelial cancers, as well as in tumor angiogenesis. COX-2 inhibitors have been shown to have anti-tumor activity in experimental cancer. Little information exists, however, on the expression or role of COX-2 in hematologic malignancies. We have use a variety of immunochemical assays to document expression of COX-2 in human and murine leukemias and hematopoietic cells. The factor-dependent murine cell lines FDCP1 and 32D expressed COX-2 when growing continuously in the presence of IL-3; expression declined markedly when growth fact
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15

Sevigny, Mary B., Kamara Graham, Esmeralda Ponce, Maggie C. Louie, and Kylie Mitchell. "Glycosylation of human cyclooxygenase-2 (COX-2) decreases the efficacy of certain COX-2 inhibitors." Pharmacological Research 65, no. 4 (2012): 445–50. http://dx.doi.org/10.1016/j.phrs.2012.01.001.

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16

Iñiguez, Miguel A., Carmen Punzón, and Manuel Fresno. "Induction of Cyclooxygenase-2 on Activated T Lymphocytes: Regulation of T Cell Activation by Cyclooxygenase-2 Inhibitors." Journal of Immunology 163, no. 1 (1999): 111–19. http://dx.doi.org/10.4049/jimmunol.163.1.111.

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Abstract Cyclooxygenase (COX), known to exist in two isoforms, COX-1 and COX-2, is a key enzyme in prostaglandin synthesis and the target for most nonsteroidal anti-inflammatory drugs. In this study, we show that human T lymphocytes express the COX-2 isoenzyme. COX-2 mRNA and protein were induced in both Jurkat and purified T cells stimulated by TCR/CD3 or PMA activation. COX-2 mRNA was induced very early after activation and superinduced by protein synthesis inhibitors, whereas it was inhibited by the immunosuppressive drug cyclosporin A, identifying it as an early T cell activation gene. Int
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17

Brown, Joanne R., and Raymond N. DuBois. "COX-2: A Molecular Target for Colorectal Cancer Prevention." Journal of Clinical Oncology 23, no. 12 (2005): 2840–55. http://dx.doi.org/10.1200/jco.2005.09.051.

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Cyclooxygenase (COX), a key enzyme in the prostanoid biosynthetic pathway, has received considerable attention due to its role in human cancers. Observational and randomized controlled studies in many different population cohorts and settings have demonstrated protective effects of nonsteroidal anti-inflammatory drugs (NSAIDs; the inhibitors of COX activity) for colorectal cancers (CRCs). COX-2, the inducible isoform of cyclooxygenase, is overexpressed in early and advanced CRC tissues, which portends a poor prognosis. Experimental studies have thus identified important mechanisms and pathways
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18

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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19

Dhir, Ashish, Pattipati Naidu, and Shrinivas Kulkarni. "Protective effect of cyclooxygenase-2 (COX-2) inhibitors but not non-selective cyclooxygenase (COX)-inhibitors on ethanol withdrawal-induced behavioural changes." Addiction Biology 10, no. 4 (2005): 329–35. http://dx.doi.org/10.1080/13556210500352964.

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20

Longo, W., B. Erickson, J. Mazuski, N. Panesar, Y. Deshpande, and D. Kaminski. "Cellular mitogenesis is inhibited by selective cyclooxygenase-2 (Cox-2) inhibitors." Gastroenterology 114 (April 1998): A636. http://dx.doi.org/10.1016/s0016-5085(98)82601-2.

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21

Al-Hourani, Baker Jawabrah, Sai Kiran Sharma, Mavanur Suresh, and Frank Wuest. "Novel 5-substituted 1H-tetrazoles as cyclooxygenase-2 (COX-2) inhibitors." Bioorganic & Medicinal Chemistry Letters 22, no. 6 (2012): 2235–38. http://dx.doi.org/10.1016/j.bmcl.2012.01.093.

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22

Marot, Christophe, Philippe Chavatte, and Daniel Lesieur. "Comparative Molecular Field Analysis of Selective Cyclooxygenase-2 (COX-2) Inhibitors." Quantitative Structure-Activity Relationships 19, no. 2 (2000): 127–34. http://dx.doi.org/10.1002/1521-3838(200004)19:2<127::aid-qsar127>3.0.co;2-p.

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23

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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24

Dickens, David S., Rafal Kozielski, Javed Khan, Anne Forus, and Timothy P. Cripe. "Cyclooxygenase-2 Expression in Pediatric Sarcomas." Pediatric and Developmental Pathology 5, no. 4 (2002): 356–64. http://dx.doi.org/10.1007/s10024-002-0005-1.

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Therapies for metastatic pediatric sarcomas have reached maximum tolerated doses, but continue to provide suboptimal cure rates. Additionally, these treatments are associated with numerous short- and long-term side effects. Therefore, the search for newer, less toxic therapeutic agents is warranted. Overexpression of the inducible enzyme, cyclooxygenase-2 (COX-2), has been discovered in a variety of adult solid tumors and numerous studies have shown COX-2 inhibitors to have significant antiproliferative effects. Therefore, we sought to determine the expression of COX-2 in pediatric sarcomas. W
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25

Wang, Zhen, Jun-qiang Chen, and Jin-lu Liu. "COX-2 Inhibitors and Gastric Cancer." Gastroenterology Research and Practice 2014 (2014): 1–7. http://dx.doi.org/10.1155/2014/132320.

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The evidence that cyclooxygenase-2 (COX-2) is upregulated and plays an important role in carcinogenesis of gastric cancer has triggered the topic of COX-2 inhibitors as chemopreventive agents for gastric cancer. Studies find that COX-2 inhibitors are associated not only with chemoprophylactic effects, but also with chemotherapeutic potentials in gastric cancer. Both COX-dependent and COX-independent pathways have a role in the anticancer efficiency of COX-2 inhibitors. However, enthusiasm is thwarted by the potential toxicity, that is, gastrointestinal toxicity of nonselective COX-2 inhibitors
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26

Vernieri, Ermelinda, Isabel Gomez-Monterrey, Ciro Milite, et al. "Design, Synthesis, and Evaluation of New Tripeptides as COX-2 Inhibitors." Journal of Amino Acids 2013 (February 26, 2013): 1–7. http://dx.doi.org/10.1155/2013/606282.

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Cyclooxygenase (COX) is a key enzyme in the biosynthetic pathway leading to the formation of prostaglandins, which are mediators of inflammation. It exists mainly in two isoforms COX-1 and COX-2. The conventional nonsteroidal anti-inflammatory drugs (NSAIDs) have gastrointestinal side effects because they inhibit both isoforms. Recent data demonstrate that the overexpression of these enzymes, and in particular of cyclooxygenases-2, promotes multiple events involved in tumorigenesis; in addition, numerous studies show that the inhibition of cyclooxygenases-2 can delay or prevent certain forms o
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27

Keshwar, Shashi, Sonal Grover, Daya Shankar, and Deependra Prasad Sarraf. "Oral cancer chemoprevention: COX-2 inhibitor a covenant." International Journal of Scientific Reports 7, no. 4 (2021): 253. http://dx.doi.org/10.18203/issn.2454-2156.intjscirep20211043.

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&lt;p&gt;Oral cancer survival remains poor despite advancement in treatment modalities. In oral cancer and oral premalignant lesions, cyclooxygenase-2 (COX-2) is widely expressed and tends to be enhanced especially in high-risk oral lesions. Numerous researches suggests that the inflammation pathway of cyclooxygenase/prostaglandin E2 (PGE2) leads to the development and progression of a number of cancers, including oral squamous cell carcinoma (OSCC). With an emphasis on research data, this article discusses the relationship between inflammation and cancer, summarizes the use of anti-inflammato
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28

Fosslien, Egil. "Biochemistry of Cyclooxygenase (COX)-2 Inhibitors and Molecular Pathology of COX-2 in Neoplasia." Critical Reviews in Clinical Laboratory Sciences 37, no. 5 (2000): 431–502. http://dx.doi.org/10.1080/10408360091174286.

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29

Fujimura, Takashi, Tetsuo Ohta, Katsunobu Oyama, Tomoharu Miyashita, and Kochi Miwa. "Cyclooxygenase-2 (COX-2) in Carcinogenesis and Selective COX-2 Inhibitors for Chemoprevention in Gastrointestinal Cancers." Journal of Gastrointestinal Cancer 38, no. 2-4 (2007): 78–82. http://dx.doi.org/10.1007/s12029-008-9035-x.

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30

Ebert, Andreas D., Julia Bartley, and Matthias David. "Aromatase inhibitors and cyclooxygenase-2 (COX-2) inhibitors in endometriosis: New questions—old answers?" European Journal of Obstetrics & Gynecology and Reproductive Biology 122, no. 2 (2005): 144–50. http://dx.doi.org/10.1016/j.ejogrb.2005.04.017.

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31

Selvaraj, Jayaraman. "Molecular docking analysis of COX-2 for potential inhibitors." Bioinformation 16, no. 10 (2020): 753–58. http://dx.doi.org/10.6026/97320630016753.

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Cyclooxygenase-2 (COX-2) is liked with breast cancer. Therefore, it is of interest to design and develop new yet effective compounds against COX-2 from medicinal plants such as the natural alkaloid compounds. We document the optimal binding features of aristolochicacid with COX-2 protein for further consideration.
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32

Cheng, Hui-Fang, Jun-Ling Wang, Ming-Zhi Zhang, James A. McKanna, and Raymond C. Harris. "Nitric oxide regulates renal cortical cyclooxygenase-2 expression." American Journal of Physiology-Renal Physiology 279, no. 1 (2000): F122—F129. http://dx.doi.org/10.1152/ajprenal.2000.279.1.f122.

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We have previously shown that cyclooxygenase-2 (COX-2) is localized to the cortical thick ascending limb of the loop of Henle (cTALH)/macula densa of the rat kidney, and expression increases in response to low-salt diet and/or angiotensin-converting enzyme (ACE) inhibition. Because of the localization of neuronal nitric oxide synthase (nNOS) to macula densa and surrounding cTALH, the present study investigated the role of nitric oxide (NO) in the regulation of COX-2 expression. For in vivo studies, rats were fed a normal diet, low-salt diet or low-salt diet combined with the ACE inhibitor capt
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33

Listyani, Tiara Ajeng, Muniroh Addawiyyah, Danang Raharjo, and Pang Jyh Chyang. "Docking and Structural Modification of Flavonoid Derivative Compounds as Cycloxygenas-2 Enzyme Inhibitors." Indonesian Journal of Global Health Research 7, no. 1 (2024): 311–22. http://dx.doi.org/10.37287/ijghr.v7i1.4041.

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Seven flavonoid compounds have the activity of inhibiting the cyclooxygenase-2 (COX-2) enzyme, thus providing an anti-inflammatory effect. Molecular docking analysis is needed to determine the binding interaction between flavonoid compounds and the cyclooxygenase-2 (COX-2) enzyme. Objective: This study aims to determine the interaction of flavonoid compounds with the cyclooxygenase-2 (COX-2) enzyme along with the modification of the flavonoid compound structure to increase the binding energy to the cyclooxygenase-2 (COX-2) enzyme. Method: Flavonoid derivative compounds were geometry optimized
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34

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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35

Pereira, Ricardo. "Selective Cyclooxygenase-2 (COX-2) Inhibitors Used for Preventing or Regressing Cancer." Recent Patents on Anti-Cancer Drug Discovery 4, no. 2 (2009): 157–63. http://dx.doi.org/10.2174/157489209788452849.

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36

Milas, Luka. "Cyclooxygenase-2 (COX-2) enzyme inhibitors as potential enhancers of tumor radioresponse." Seminars in Radiation Oncology 11, no. 4 (2001): 290–99. http://dx.doi.org/10.1053/srao.2001.26018.

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37

Mukherjee, Debabrata. "Selective cyclooxygenase-2 (COX-2) inhibitors and potential risk of cardiovascular events." Biochemical Pharmacology 63, no. 5 (2002): 817–21. http://dx.doi.org/10.1016/s0006-2952(02)00842-0.

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38

Kitahara, Masashi, Frank Eitner, Tammo Ostendorf, et al. "Selective Cyclooxygenase-2 Inhibition Impairs Glomerular Capillary Healing in Experimental Glomerulonephritis." Journal of the American Society of Nephrology 13, no. 5 (2002): 1261–70. http://dx.doi.org/10.1681/asn.v1351261.

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ABSTRACT. Selective cyclooxygenase-2 (COX-2) inhibitors have anti-inflammatory activity and reduce proteinuria in experimental membranous glomerulonephritis. Antiangiogenic properties of COX-2 inhibitors were recently reported. Whether these properties are relevant to the glomerular healing process in inflammatory glomerular diseases was investigated. For evaluation of the effects of selective COX-2 inhibitors on the glomerular healing process in a rat model of mesangioproliferative glomerulonephritis (induced by anti-Thy 1.1 antibody), a selective COX-2 inhibitor (rofecoxib or celecoxib) or v
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39

Tugcu, Gulcin, Hande Sipahi, and Ahmet Aydin. "Application of a Validated QSTR Model for Repurposing COX-2 Inhibitor Coumarin Derivatives as Potential Antitumor Agents." Current Topics in Medicinal Chemistry 19, no. 13 (2019): 1121–28. http://dx.doi.org/10.2174/1568026619666190618143552.

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Background: The discovery of novel potent molecules for both cancer prevention and treatment has been continuing over the past decade. In recent years, identification of new, potent, and safe anticancer agents through drug repurposing has been regarded as an expeditious alternative to traditional drug development. The cyclooxygenase-2 is known to be over-expressed in several types of human cancer. For this reason cyclooxygenase-2 inhibition may be useful tool for cancer chemotherapy. Objective: The first aim of the study was to develop a validated linear model to predict antitumor activity. Su
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40

Barrera, Ericsson David Coy, and Luis Enrique Cuca Suárez. "In vitro Inhibitory Activities of Lauraceae Aporphine Alkaloids." Natural Product Communications 5, no. 3 (2010): 1934578X1000500. http://dx.doi.org/10.1177/1934578x1000500308.

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The in vitro anti-inflammatory effect of eight aporphine alkaloids isolated from the leaves of two Lauraceae plants (Pleurothyrium cinereum and Ocotea macrophylla) was evaluated through inhibition of two isozymes of cyclooxygenase (COX-1 and COX-2), 5-lipoxygenase (5-LOX), and platelet aggregation induced by PAF, AA and ADP. All alkaloids exhibited inhibitory activities against COX-2 (IC50 25.9-116 μM range) and PAF- and AA-induced platelet aggregation, while only four and three of them were good COX-1 and 5-LOX inhibitors, respectively. (+)-N-acetyl-nornantenine 6 was the most potent COX-2, 5
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41

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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42

Zhang, Yan Ling, Yuan Ming Wang, and Yan Jiang Qiao. "Combinatorial Screening of COX-2 Inhibitors from Chinese Herbs Based on Multiple Structure-Based Pharmacophores." Advanced Materials Research 791-793 (September 2013): 269–73. http://dx.doi.org/10.4028/www.scientific.net/amr.791-793.269.

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Ten structure-based pharmacophore models of Cyclooxygenase 2 (COX-2) inhibitors were generated by LigandScout based on COX-2 inhibitor complexes from the Protein Data Bank (PDB). The potential COX-2 inhibitors were identified from traditional Chinese medicine with the method of combinatorial screening with ten models. Based on the screening results of MDDR and the metrics of E, A% and comprehensive appraisal index (CAI), the threshold of hit frequency of molecules was defined and used to identify the active molecules from Chinese herbs. The molecules hit by not less than six pharmacophore mode
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43

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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44

Macková, Anna, Pavel Mučaji, Ute Widowitz, and Rudolf Bauer. "In vitro Anti-inflammatory Activity of Ligustrum vulgare Extracts and Their Analytical Characterization." Natural Product Communications 8, no. 11 (2013): 1934578X1300801. http://dx.doi.org/10.1177/1934578x1300801102.

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Interest in the anti-inflammatory effects of Ligustrum vulgare L., which has been used traditionally in China and Japan prompted us to determine anti-inflammatory effects of the plant's compounds in leukocytes. The leaves of L. vulgare were used to prepare a decoction which was successively extracted with organic solvents (dichloromethane (DCM), n-butanol, ethyl acetate) using liquid-liquid partition. Extracts were tested for inhibition of LTB4, resp. PGE2 biosynthesis. Each extract was evaluated for its in vitro cyclooxygenase-1/2 (COX-1/2) inhibitory activity using assays with purified COX-1
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45

Jones, S. Christopher. "Relative Thromboembolic Risks Associated with COX-2 Inhibitors." Annals of Pharmacotherapy 39, no. 7-8 (2005): 1249–59. http://dx.doi.org/10.1345/aph.1e654.

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OBJECTIVE To evaluate the clinical literature on cyclooxygenase-2 (COX-2) inhibitors to determine whether a greater incidence of thromboembolic events is universal within the drug class. DATA SOURCES A MEDLINE search was conducted (1996–March 2005) for key articles in the English language assessing the efficacy or safety of these agents. STUDY SELECTION AND DATA EXTRACTION Randomized, double-blind, and controlled trials, as well as case–control and retrospective cohort studies, that assessed the cardiovascular safety of COX-2 inhibitors were reviewed. DATA SYNTHESIS Seventeen published studies
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46

Chandrakirana Krisnamurti, Gabriella, and Fatchiyah Fatchiyah. "The Biological Function Prediction of The 10-gingerol Compound of Ginger in Inhibiting Cyclooxygenase-2 Activity." Journal of Pure and Applied Chemistry Research 9, no. 3 (2020): 222–32. http://dx.doi.org/10.21776/ub.jpacr.2020.009.03.547.

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Anti-inflammatory agents inhibit prostaglandin synthesis by blocking cyclooxygenases (COXs). The compounds extracted from ginger, 10-gingerol and 10-shogaol can inhibit inflammation but the mechanism of inhibition remains unclear. Here we used molecular docking to predict the molecular interactions between COXs and the three inhibitors, acetaminophen (CID1983), 10-gingerol (CID168115) and 10-shogaol (CID6442612). By using that acetaminophen as a gold standard, the results demonstrated that acetaminophen, 10-gingerol, and 10-shogaol could bind catalytic domain and membrane binding domain of cyc
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Ifora, Ifora, Putri Aida, and Oktavia Sri. "Vitex trifolia as Cyclooxygenase-2 Inhibitors in Anti-Inflammatory Drug Discovery." International Journal Of Pharmaceutical And Bio-Medical Science 02, no. 10 (2022): 400–406. https://doi.org/10.5281/zenodo.7147501.

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<strong>ABSTRACT: </strong>Inflammation is involved in several stages of diseases such as cardiovascular diseases, asthma, diabetes, neurodegenerative diseases, or cancer. Cyclooxygenase-2 (COX-2) is an important enzyme that catalyzes the production of prostaglandins from arachidonic acid and has an important role in various inflammatory-related pathologies. The selective suppression of COX-2 over COX-1 is thought to be a useful approach for treating inflammation. <em>Vitex trifolia </em>is traditionally used for various inflammatory ailments, thus giving scope for anti-inflammatory studies. S
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48

Mitra, Manu. "Usage of COX-1 and COX-2 Nanomedicines in Nanotechnology." Nanomedicine & Nanotechnology Open Access 8, no. 3 (2023): 1–13. http://dx.doi.org/10.23880/nnoa-16000245.

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Nanomedicine is the branch of medical applications in nanotechnology. Nanomedicine ranges from medical applications of nanomaterials, biological devices to nanoelectronic biosensors, molecular nanotechnology such as biological machines. It utilizes knowledge and tools of nanotechnology to prevention and treatment of disease. Nanomedicine involves use of nanoscale materials such as biocompatible nanoparticles for delivery, sensing or actuation in a living organism. COX inhibitors are a class of pharmaceutical compounds that selectively target and inhibit the activity of the enzymes cyclooxygena
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Siriwa, Sultan Yosua, Suparto Suparto, and Rudy Ciulianto. "Efektivitas COX-2 Inhibitor Sebagai Preemptive Analgesia pada Operasi Total Knee Arthoplasty." Jurnal MedScientiae 3, no. 2 (2024): 219–26. http://dx.doi.org/10.36452/jmedscientiae.v3i2.3247.

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Nyeri pasca operasi khususnya prosedur TKA merupakan salah satu masalah yang sering ditemukan. Penggunaan analgetik adekuat merupakan tatalaksana utama untuk menekan efek samping nyeri yaitu imobilisasi, penurunan range of motion (ROM), peningkatan risiko tromboemboli dan penurunan tingkat keberhasilan rehabilitasi. Beberapa studi terdahulu melaporkan adanya kemungkinan efek terapeutik yang signifikan terhadap respon nyeri pasca operasi dengan penggunaan metode preemptive analgesia dengan cyclooxygenase-2 inhibitor (COX-2 inhibitor). Tujuan penelitian ini untuk mengetahui efektivitas COX-2 inh
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Schmassmann, Adrian, Georg Zoidl, Brigitta M. Peskar, et al. "Role of the different isoforms of cyclooxygenase and nitric oxide synthase during gastric ulcer healing in cyclooxygenase-1 and -2 knockout mice." American Journal of Physiology-Gastrointestinal and Liver Physiology 290, no. 4 (2006): G747—G756. http://dx.doi.org/10.1152/ajpgi.00416.2005.

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Traditional NSAIDs, selective cyclooxygenase (COX)-2 inhibitors, and inhibitors of nitric oxide synthase (NOS) impair the healing of preexisting gastric ulcers. However, the role of COX-1 (with or without impairment of COX-2) and the interaction between COX and NOS isoforms during healing are less clear. Thus we investigated healing and regulation of COX and NOS isoforms during ulcer healing in COX-1 and COX-2 deficiency and inhibition mouse models. In this study, female wild-type COX-1−/− and COX-2−/− mice with gastric ulcers induced by cryoprobe were treated intragastrically with vehicle, se
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