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Journal articles on the topic 'Coxib'

Author: Grafiati

Published: 4 June 2021

Last updated: 25 July 2025

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1

Vio, Carlos P., Mariana Quiroz-Munoz, Catherina A. Cuevas, Carlos Cespedes, and Nicholas R. Ferreri. "Prostaglandin E2 EP3 receptor regulates cyclooxygenase-2 expression in the kidney." American Journal of Physiology-Renal Physiology 303, no. 3 (2012): F449—F457. http://dx.doi.org/10.1152/ajprenal.00634.2011.

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Cyclooxygenase-2 (COX-2) is constitutively expressed and highly regulated in the thick ascending limb (TAL). As COX-2 inhibitors (Coxibs) increase COX-2 expression, we tested the hypothesis that a negative feedback mechanism involving PGE2 EP3 receptors regulates COX-2 expression in the TAL. Sprague-Dawley rats were treated with a Coxib [celecoxib (20 mg·kg−1·day−1) or rofecoxib (10 mg·kg−1·day−1)], with or without sulprostone (20 μg·kg−1·day−1). Sulprostone was given using two protocols, namely, previous to Coxib treatment (prevention effect; Sulp7-Coxib5 group) and 5 days after initiation of

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2

Gross, Manfred. "NSAR, Coxibe und Steroide: Wann und wie sollten Magen und Darm geschützt werden?" Aktuelle Rheumatologie 42, no. 06 (2017): 497–504. http://dx.doi.org/10.1055/s-0043-110009.

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ZusammenfassungNicht-steroidale Antirheumatika (NSAR) haben ein hohes Risiko für gastrointestinale Komplikationen wie Ulzera, Ulkusblutungen oder Perforationen. Zudem verspüren 25-30% der Patienten Oberbauchbeschwerden (Dyspepsie). Die PPI-Komedikation zu einem NSAR kann die Rate an Ulzera, Blutungen und sonstigen Komplikationen sowie die Dyspepsierate senken. Ein anderer Ansatz zur Erhöhung der Sicherheit der Therapie ist die Verschreibung eines Cox-2-spezifischen NSAR (Coxib). Unter Coxiben treten seltener gastrointestinale Komplikationen einer NSAR-Therapie auf.Die beiden präventiven Strate

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3

Hunt, Richard H., Alan N. Barkun, David Baron, et al. "Recommendations for the Appropriate Use of Anti-Inflammatory Drugs in the Era of the Coxibs: Defining the Role of Gastroprotective Agents." Canadian Journal of Gastroenterology 16, no. 4 (2002): 231–40. http://dx.doi.org/10.1155/2002/516092.

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Treatment with anti-inflammatory drugs and the analgesic efficacy of conventional nonsteroidal anti-inflammatory drugs (NSAIDs) are compromised by a two- to fourfold increased risk of gastrointestinal complications. This increased risk has resulted in an increasing use of the new selective cyclooxygenase-2 inhibitors or coxibs, which, in clinical trials and outcomes studies, reduced gastrointestinal adverse events by 50% to 65% compared with conventional NSAIDs. However, the coxibs are not available to all patients who need them, and NSAIDs are still widely used. Moreover, treatment with a cox

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4

Yan, Brian, Yvette Leung, Stefan J. Urbanski, and Robert P. Myers. "Rofecoxib-Induced Hepatotoxicity: A Forgotten Complication of the Coxibs." Canadian Journal of Gastroenterology 20, no. 5 (2006): 351–55. http://dx.doi.org/10.1155/2006/356434.

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Rofecoxib is a member of the coxib family of nonsteroidal anti-inflammatory drugs that selectively inhibit cyclooxygenase-2. Although the coxibs are generally well-tolerated, rofecoxib was recently withdrawn from the market due to concerns regarding cardiovascular safety. Rare cases of hepatic injury attributable to the coxibs have been reported. In the present study, two additional cases of severe hepatotoxicity are described in patients with cholestatic symptoms and abnormal liver biochemistry, shortly following the initiation of rofecoxib for arthritic complaints. In both cases, liver histo

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5

Ghosh, Mallika, Haibin Wang, Youxi Ai та ін. "COX-2 suppresses tissue factor expression via endocannabinoid-directed PPARδ activation". Journal of Experimental Medicine 204, № 9 (2007): 2053–61. http://dx.doi.org/10.1084/jem.20070828.

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Although cyclooxygenase (COX)-2 inhibitors (coxibs) are effective in controlling inflammation, pain, and tumorigenesis, their use is limited by the recent revelation of increased adverse cardiovascular events. The mechanistic basis of this side effect is not well understood. We show that the metabolism of endocannabinoids by the endothelial cell COX-2 coupled to the prostacyclin (PGI2) synthase (PGIS) activates the nuclear receptor peroxisomal proliferator–activated receptor (PPAR) δ, which negatively regulates the expression of tissue factor (TF), the primary initiator of blood coagulation. C

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6

Dembo, Gregory, Sang B. Park, and Evan D. Kharasch. "Central Nervous System Concentrations of Cyclooxygenase-2 Inhibitors in Humans." Anesthesiology 102, no. 2 (2005): 409–15. http://dx.doi.org/10.1097/00000542-200502000-00026.

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Background Cyclooxygenase-2 (COX-2)-selective inhibitors (coxibs) are under investigation for the potential therapy, attenuation, or prevention of neuroinflammatory and neurodegenerative disorders. Coxibs are also a significant advance in pain therapy and are traditionally considered to achieve analgesia via peripheral effects. However, in animals, central nervous system (CNS) COX-2 activity and prostanoid concentrations are increased by peripheral inflammation, central sensitization has been proposed to account for long-term pain-related phenomena, and coxibs achieve significant cerebrospinal

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7

Ribaldone, Davide Giuseppe. "Coxib Safety in Patients with Inflammatory Bowel Diseases: A Meta-analysis." Pain Physician 6;18, no. 6;11 (2015): 599–607. http://dx.doi.org/10.36076/ppj.2015/18/599.

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Background: Patients with inflammatory bowel diseases (IBD) frequently have extraintestinal manifestations including arthritis, sacroiliitis, and ankylosing spondylitis. While the treatment of these rheumatological conditions with traditional non-steroidal anti-inflammatory drugs (NSAIDs) has been reported to lead to frequent IBD exacerbation, the safety of cyclooxygenase-2 (COX-2) inhibitors (Coxibs) remains unclear. Objectives: Our aim is to carry out a meta-analysis to verify if Coxibs, employed to treat rheumatological manifestations, are associated with an increased risk of exacerbation o

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8

Whelton, Andrew. "The Coxib Conundrum." American Journal of Therapeutics 11, no. 6 (2004): 417–21. http://dx.doi.org/10.1097/01.mjt.0000149719.58535.b0.

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9

Schmutz, J. L., A. Barbaud, and P. Trechot. "Pseudoporphyrie et Coxib." Annales de Dermatologie et de Vénéréologie 133, no. 2 (2006): 213. http://dx.doi.org/10.1016/s0151-9638(06)70881-x.

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10

Seta, Francesca, Andrew D. Chung, Patricia V. Turner, Jeffrey D. Mewburn, Ying Yu, and Colin D. Funk. "Renal and cardiovascular characterization of COX-2 knockdown mice." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 296, no. 6 (2009): R1751—R1760. http://dx.doi.org/10.1152/ajpregu.90985.2008.

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Selective cyclooxygenase-2 (COX-2) inhibitors (coxibs) increase the incidence of cardiovascular and cerebrovascular events. Complete disruption of the murine gene encoding COX-2 ( Ptgs2) leads to renal developmental problems, as well as female reproductive anomalies and patent ductus arteriosus of variable penetrance in newborns, thus rendering this genetic approach difficult to compare with coxib administration. Here, we created hypomorphic Ptgs2 (COX-2Neo/Neo) mice in which COX-2 expression is suppressed to an extent similar to that achieved with coxibs, but not eliminated, in an attempt to

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11

Cantor, Scott B. "Pharmacoeconomics of Coxib Therapy." Journal of Pain and Symptom Management 24, no. 1 (2002): S28—S37. http://dx.doi.org/10.1016/s0885-3924(02)00412-8.

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12

Rainsford, K. D. "Introduction — The coxib controversies." InflammoPharmacology 13, no. 4 (2005): 331–41. http://dx.doi.org/10.1163/156856005774415628.

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13

Broich, Karl, and Hans-Karl Heim. "Selective COX-2 inhibitors and risk of thromboembolic events – regulatory aspects." Thrombosis and Haemostasis 96, no. 10 (2006): 423–32. http://dx.doi.org/10.1160/th06-08-0462.

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SummaryIn the 1990s, the pharmaceutical industry developed selective COX-2 inhibitors (coxibs) as alternatives to conventional nonsteroidal anti-inflammatory drugs (NSAIDs), with the expectation of similar analgetic and anti-inflammatory efficacy but a reduced risk of adverse gastrointestinal (GI) effects. Marketing authorisation (MA) was granted for rofecoxib and celecoxib as first representatives of this new pharmacological class at the end of the 1990s in the EU. In the following years MAs were granted for the ´second generation` coxibs etoricoxib, parecoxib/valdecoxib and lumiracoxib. Howe

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14

Hermann. "Kardiovaskuläres Risiko von nicht-steroidalen Antirheumatika." Praxis 101, no. 20 (2012): 1309–14. http://dx.doi.org/10.1024/1661-8157/a001074.

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Die klassischen nicht-selektiven nicht-steroidalen Antirheumatika (NSAR) und die neueren selektiven Cyclooxygenase-2-Hemmer (Coxibe) werden seit vielen Jahrzehnten erfolgreich bei Patienten mit chronischen Schmerzzuständen eingesetzt. Neben den bekannten gastrointestinalen (NSAR) und renalen (NSAR, Coxibe) Nebenwirkungen sind in den letzten Jahren auch die kardiovaskulären Risiken dieser Medikamente vermehrt wahrgenommen worden. Dieses Risiko ist für alle Vertreter dieser beiden Medikamentenklassen erhöht und kann unter anderem durch Erhöhung des Blutdruckes und Beeinträchtigung der vaskulären

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15

Lema, M. J. "Emerging options with coxib therapy." Cleveland Clinic Journal of Medicine 69, Suppl_1 (2002): SI76. http://dx.doi.org/10.3949/ccjm.69.suppl_1.si76.

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16

Einecke, Dirk. "Coxib besser als NSAR plus PPI." MMW - Fortschritte der Medizin 152, no. 25-27 (2010): 1. http://dx.doi.org/10.1007/bf03366750.

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17

Einecke, Ursula. "Coxib sicherer als NSAR plus Säurehemmer." MMW - Fortschritte der Medizin 152, no. 31-33 (2010): 50. http://dx.doi.org/10.1007/bf03366897.

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18

Maronde, Ulrike. "Coxib schonender als NSAR plus Säurehemmer." MMW - Fortschritte der Medizin 152, no. 44 (2010): 103. http://dx.doi.org/10.1007/bf03367336.

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19

FINN, ROBERT. "PPI Cotherapy Matches Coxib for Gastroprotection." Ob.Gyn. News 42, no. 18 (2007): 27. https://doi.org/10.1016/s0029-7437(07)70828-5.

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20

Hugo F. Miranda, Viviana Noriega, Francisca Moreno, Fernando Sierralta, Ramón Sotomayor-Zárate, and Juan Carlos Prieto. "Nitridergic Modulation of COX-2 Efficacy." World Journal of Advanced Research and Reviews 15, no. 2 (2022): 044–51. http://dx.doi.org/10.30574/wjarr.2022.15.2.0784.

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Pain is a common unpleasant sensory and emotional experience, in which are frequently used in their treatment the nonsteroidal anti-inflammatory drugs (NSAIDs). A group of agents with antipyretic, analgesic, and anti-inflammatory properties due to the inhibition of cyclooxygenase enzymes (COXs). Among these drugs there are a group of selective inhibitors of COX-2 named coxib that include to parecoxib, celecoxib, rofecoxib and etoricoxib. Pharmacological information on the mechanism of action of coxibs is insufficient to determine the analgesic and anti-inflammatory efficacy of these agents. Th

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21

Hugo, F. Miranda, Noriega Viviana, Moreno Francisca, Sierralta Fernando, Sotomayor-Zárate Ramón, and Carlos Prieto Juan. "Nitridergic Modulation of COX-2 Efficacy." World Journal of Advanced Research and Reviews 15, no. 2 (2022): 044–51. https://doi.org/10.5281/zenodo.7750983.

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Pain is a common unpleasant sensory and emotional experience, in which are frequently used in their treatment the nonsteroidal anti-inflammatory drugs (NSAIDs). A group of agents with antipyretic, analgesic, and anti-inflammatory properties due to the inhibition of cyclooxygenase enzymes (COXs). Among these drugs there are a group of selective inhibitors of COX-2 named coxib that include to parecoxib, celecoxib, rofecoxib and etoricoxib. Pharmacological information on the mechanism of action of coxibs is insufficient to determine the analgesic and anti-inflammatory efficacy of these agents. Th

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22

Greenberg, Jeffrey D., Clifton O. Bingham, Steven B. Abramson, et al. "Assessment of coxib utilization by rheumatologists for nonsteroidal antiinflammatory drug gastroprotection prior to the coxib market withdrawals." Arthritis & Rheumatism 55, no. 4 (2006): 543–50. http://dx.doi.org/10.1002/art.22095.

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23

de Carlos, F., J. Cobo, C. Perillan, et al. "Orthodontic tooth movement after different coxib therapies." European Journal of Orthodontics 29, no. 6 (2007): 596–99. http://dx.doi.org/10.1093/ejo/cjm072.

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24

Misak, A. "Coxib medications to be handled with care." Canadian Medical Association Journal 172, no. 3 (2005): 330. http://dx.doi.org/10.1503/cmaj.045313.

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25

Bonn, Dorothy. "Non-coxib celecoxib derivative arrests myeloma cells." Lancet Oncology 6, no. 10 (2005): 740. http://dx.doi.org/10.1016/s1470-2045(05)70373-9.

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26

Gross, M. "Coxib plus PPI verhindert Ulzera am besten." MMW - Fortschritte der Medizin 158, no. 17 (2016): 40. http://dx.doi.org/10.1007/s15006-016-8773-0.

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27

Schönthal, Axel H. "Antitumor properties of dimethyl-celecoxib, a derivative of celecoxib that does not inhibit cyclooxygenase-2: implications for glioma therapy." Neurosurgical Focus 20, no. 4 (2006): E21. http://dx.doi.org/10.3171/foc.2006.20.4.14.

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✓ Celecoxib (Celebrex) appears to be unique among the class of selective COX-2 inhibitors (coxibs), because this particular compound exerts a second function that is independent of its celebrated ability to inhibit COX-2. This second function is the potential to inhibit cell proliferation and stimulate apoptotic cell death at much lower concentrations than any other coxibs. Intriguingly, these two functions are mediated by different moieties of the celecoxib molecule and can be separated. The author, as well as others, have generated and investigated analogs of celecoxib that retain only one o

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28

&NA;. "Comparing nimesulide- and coxib-associated ADRs in India." Reactions Weekly &NA;, no. 995 (2004): 4. http://dx.doi.org/10.2165/00128415-200409950-00008.

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29

Okie, Susan. "Raising the Safety Bar — The FDA's Coxib Meeting." New England Journal of Medicine 352, no. 13 (2005): 1283–85. http://dx.doi.org/10.1056/nejmp058055.

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30

Cohen, E. J. "Rasing the Safety Bar — The FDA's Coxib Meeting." Yearbook of Ophthalmology 2006 (January 2006): 276–78. http://dx.doi.org/10.1016/s0084-392x(08)70414-3.

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31

Dieppe, Paul. "Complicity Theory: An Explanation for the ‘Coxib Problem’?" Journal of the Royal Society of Medicine 99, no. 6 (2006): 273–74. http://dx.doi.org/10.1177/014107680609900603.

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32

Califf, Robert M. "The coxib story: some lessons and more questions." American Journal of Cardiology 89, no. 8 (2002): 971–72. http://dx.doi.org/10.1016/s0002-9149(02)02249-x.

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33

Herrmann, Matthias. "Entzündungsbedingte Schmerzen: Coxib schützt auch den unteren Verdauungstrakt." Angewandte Schmerztherapie und Palliativmedizin 5, no. 3 (2012): 51. http://dx.doi.org/10.1007/s15223-012-0122-2.

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34

Santilli, Francesca, Andrea Boccatonda, Giovanni Davì, and Francesco Cipollone. "The Coxib case: Are EP receptors really guilty?" Atherosclerosis 249 (June 2016): 164–73. http://dx.doi.org/10.1016/j.atherosclerosis.2016.04.004.

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35

Dieppe, P. "Complicity theory: an explanation for the `coxib problem'?" Journal of the Royal Society of Medicine 99, no. 6 (2006): 273–74. http://dx.doi.org/10.1258/jrsm.99.6.273.

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36

Gumułka, Paweł, Monika Dąbrowska, and Małgorzata Starek. "Stability Study of Selected Coxibs Used in the Treatment of Rheumatoid Diseases in Various Drug Combinations." Processes 11, no. 9 (2023): 2605. http://dx.doi.org/10.3390/pr11092605.

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Coxibs are a group of non-steroidal anti-inflammatory drugs (NSAIDs), selective cyclooxygenase 2 inhibitors, characterized by a much lower gastrotoxicity compared to classic NSAIDs. They are often used in conjunction with other drugs, which greatly increases the likelihood of adverse drug interactions. The presented study analyzed the degradation rate of celecoxib and cimicoxib in solutions under the influence of other medicinal substances at different temperatures. For this purpose, triple-drug mixtures were prepared, consisting of coxib and eleven different commonly used drugs (paracetamol,

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37

Russo, Pierluigi, Luca Degli Esposti, Alessandro Capone, Ezio Degli Esposti, and Luciano Caprino. "Farmacoeconomia dei COXIB nella patologia osteoarticolare: revisione della letteratura." Farmeconomia. Health economics and therapeutic pathways 4, no. 1S (2003): 5–13. http://dx.doi.org/10.7175/fe.v4i1s.1032.

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A new class of anti-inflammatory agents, the selective inhibitors of cyclooxygenase-2 (COXIBs), has been recently introduced into the market for the treatment of osteoarthritis and reumatoid arthritis. Randomized and controlled clinical trials showed a similar efficacy and a better tolerability profile of COXIBs compared with conventional non-steroidal anti-inflammatory drugs (NSAIDs). The aim of this study was to perform a scientific literature review relating to the economic impact produced by COXIBs’ introduction. The research of references included the following databases: MEDLINE, EMBASE

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38

FINN, ROBERT. "PPI Plus NSAID Provides Same Gastroprotection as a Coxib." Family Practice News 37, no. 20 (2007): 37. http://dx.doi.org/10.1016/s0300-7073(07)71266-5.

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39

Topol, Eric J., and Gary W. Falk. "A coxib a day won't keep the doctor away." Lancet 364, no. 9435 (2004): 639–40. http://dx.doi.org/10.1016/s0140-6736(04)16906-7.

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40

Marnett, Lawrence J. "The COXIB Experience: A Look in the Rearview Mirror." Annual Review of Pharmacology and Toxicology 49, no. 1 (2009): 265–90. http://dx.doi.org/10.1146/annurev.pharmtox.011008.145638.

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41

Scott, David. "Prexige: new coxib for OA, dysmenorrhoea and acute pain." Prescriber 17, no. 18 (2006): 49–54. http://dx.doi.org/10.1002/psb.422.

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42

Reiss, Allison B., Farah Anwar, Edwin S. L. Chan, and Kamran Anwar. "Disruption of Cholesterol Efflux by Coxib Medications and Inflammatory Processes." Journal of Investigative Medicine 57, no. 6 (2009): 695–702. http://dx.doi.org/10.2310/jim.0b013e31819ec3c7.

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43

Sperandio da Silva, Gilberto M., Lidia M. Lima, Carlos A. M. Fraga, Carlos M. R. Sant’Anna та Eliezer J. Barreiro. "The molecular basis for coxib inhibition of p38α MAP kinase". Bioorganic & Medicinal Chemistry Letters 15, № 15 (2005): 3506–9. http://dx.doi.org/10.1016/j.bmcl.2005.05.107.

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44

Dr., V. Kumaran, S. M. Vignesh Prasad Dr., and Sasirekha Dr. "Effects of COXIB in Orthodontic Tooth Movement – A Literature Review." International Journal of Research and Review 6, no. 1 (2019): 73–82. https://doi.org/10.5281/zenodo.3984762.

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Pain measurements help to determine the severity, type and duration of pain and are used to make an accurate diagnosis and evaluate the effectiveness of treatment. Pain relief can be achieved pharmacologically or non pharmacologically. Pharmacologically, NSAIDs are the drugs of choice. They act by inhibition of enzyme cyclooxygenase which mediates the transformation of prostaglandins from arachidonic acid in the cellular plasma membrane. PGs such as PGE and PGE2 are important mediators of bone resorption. COX – 1 is considered important in tissue homeostasis. COX – 2 is transcripti

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45

Scribbans, Trisha D., Brittany A. Edgett, Jacob T. Bonafiglia, Brittany L. Baechler, Joe Quadrilatero, and Brendon J. Gurd. "A systematic upregulation of nuclear and mitochondrial genes is not present in the initial postexercise recovery period in human skeletal muscle." Applied Physiology, Nutrition, and Metabolism 42, no. 6 (2017): 571–78. http://dx.doi.org/10.1139/apnm-2016-0455.

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The purpose of the current investigation was to determine if an exercise-mediated upregulation of nuclear and mitochondrial-encoded genes targeted by the transcriptional co-activator peroxisome-proliferator-activated receptor gamma co-activator-1 alpha (PGC-1α) occurs in a systematic manner following different exercise intensities in humans. Ten recreationally active males (age: 23 ± 3 years; peak oxygen uptake: 41.8 ± 6.6 mL·kg−1·min−1) completed 2 acute bouts of work-matched interval exercise at ∼73% (low; LO) and ∼100% (high; HI) of work rate at peak oxygen uptake in a randomized crossover

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46

Neuber, Christin, Luisa Niedenzu, Sabine Schulze, et al. "Exploring a Nitric Oxide-Releasing Celecoxib Derivative as a Potential Modulator of Bone Healing: Insights from Ex Vivo and In Vivo Imaging Experiments." International Journal of Molecular Sciences 26, no. 6 (2025): 2582. https://doi.org/10.3390/ijms26062582.

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The inducible enzyme cyclooxygenase-2 (COX-2) and the subsequent synthesis of eicosanoids initiated by this enzyme are important molecular players in bone healing. In this pilot study, the suitability of a novel selective COX-2 inhibitor bearing a nitric oxide (NO)-releasing moiety was investigated as a modulator of healing a critical-size bone defect in rats. A 5 mm femoral defect was randomly filled with no material (negative control, NC), a mixture of collagen and autologous bone fragments (positive control, PC), or polycaprolactone-co-lactide (PCL)-scaffolds coated with two types of artifi

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47

Kim. "A BRIEF OVERVIEW OF THE COXIB DRUGS IN THE VETERINARY FIELD." American Journal of Animal and Veterinary Sciences 8, no. 2 (2013): 89–97. http://dx.doi.org/10.3844/ajavsp.2013.89.97.

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48

Bergh, Mary Sarah, and Steven C. Budsberg. "The Coxib NSAIDs: Potential Clinical and Pharmacologic Importance in Veterinary Medicine." Journal of Veterinary Internal Medicine 19, no. 5 (2005): 633–43. http://dx.doi.org/10.1111/j.1939-1676.2005.tb02741.x.

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49

Laine, Loren, Laurine G. Connors, Alise Reicin, et al. "Serious lower gastrointestinal clinical events with nonselective NSAID or coxib use." Gastroenterology 124, no. 2 (2003): 288–92. http://dx.doi.org/10.1053/gast.2003.50054.

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50

Meador, Robert, and Sharon Kolasinski. "Acute Renal Failure Can Occur with Inappropriate Use of a Coxib." JCR: Journal of Clinical Rheumatology 7, no. 6 (2001): 413–14. http://dx.doi.org/10.1097/00124743-200112000-00017.

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