Celecoxib Systematic (IUPAC) name 4-[5-(4-methylphenyl)-3-(trifluoromethyl)
Clinical data Trade names Celebrex AHFS/Drugs.com MedlinePlus Pregnancy cat. B3(AU) C(US) Legal status ℞ Prescription only Routes Oral Pharmacokinetic data Bioavailability 40% Protein binding 97% (mainly to serum albumin) Metabolism Hepatic (mainly CYP2C9) Half-life ~11 h Excretion Renal 27%, faecal 57% Identifiers CAS number ATC code L01 M01 PubChem DrugBank ChemSpider UNII KEGG ChEBI ChEMBL Chemical data Formula C17H14F3N3O2S Mol. mass 381.373 g/mol SMILES & (what is this?)
Celecoxib INN ( //) is a sulfa non-steroidal anti-inflammatory drug (NSAID) and selective COX-2 inhibitor used in the treatment of osteoarthritis, rheumatoid arthritis, acute pain, painful menstruation and menstrual symptoms, and to reduce numbers of colon and rectum polyps in patients with familial adenomatous polyposis. It is marketed by Pfizer. It is known under the brand name Celebrex or Celebra for arthritis and Onsenal for polyps. Celecoxib is available by prescription in capsule form.
Celecoxib is licensed for use in osteoarthritis, rheumatoid arthritis, acute pain, painful menstruation and menstrual symptoms, ankylosing spondylitis and to reduce the number of colon and rectal polyps in patients with familial adenomatous polyposis. It was originally intended to relieve pain while minimizing the gastrointestinal adverse effects usually seen with conventional NSAIDs. In practice, its primary indication is in patients who need regular and long term pain relief: there is probably no advantage to using celecoxib for short term or acute pain relief over conventional NSAIDs, except in the situation where non-selective NSAIDs or aspirin cause cutaneous reactions (urticaria or "hives"). In addition, the pain relief offered by celecoxib is similar to that offered by paracetamol (acetaminophen).
Fabricated efficacy studies
On March 11, 2009, Scott S. Reuben, former chief of acute pain at Baystate Medical Center, Springfield, Mass., revealed that data for 21 studies he had authored for the efficacy of the drug (along with others such as Vioxx) had been fabricated, the analgesic effects of the drugs being exaggerated. Dr. Reuben was also a former paid spokesperson for Pfizer. The retracted studies were not submitted to either the U.S. Food and Drug Administration or the European Union's regulatory agencies prior to the drug's approval. Pfizer issued a public statement declaring, "It is very disappointing to learn about Dr. Scott Reuben's alleged actions. When we decided to support Dr. Reuben's research, he worked for a credible academic medical center and appeared to be a reputable investigator." 
Pfizer sells celecoxib under the brand name Celebrex, and is available as oral capsules containing 50 mg, 100 mg, 200 mg or 400 mg of celecoxib.
Celecoxib is not currently available as a generic in the United States, because it is covered by unexpired Pfizer patents. However, in other countries, including India and the Philippines, it is legally available as a generic under the brand names Cobix', Celcoxx and Celexib.
The usual adult dose of celecoxib is 100 to 200 mg once or twice a day. The lowest effective dose should be used.
In theory the COX-2 selectivity should result in a significantly lower incidence of gastrointestinal ulceration than traditional NSAIDs. The main items of evidence cited to support this theory were the preliminary (6 month) results of the Celecoxib Long-term Arthritis Safety Study (CLASS) as published in 2000, which demonstrated a significant reduction in the combination of symptomatic ulcers plus ulcer complications in those taking celecoxib versus ibuprofen or diclofenac, provided they were not on aspirin (Silverstein et al., 2000). However, this was not significant at 12 months (full study length).
Patients with prior history of ulcer disease or GI bleeding. Moderate to severe hepatic impairment, GI toxicity can occur with or without warning symptoms in patients treated with NSAIDs
Celecoxib contains a sulfonamide moiety and may cause allergic reactions in those allergic to other sulfonamide-containing drugs. This is in addition to the contraindication in patients with severe allergies to other NSAIDs. However, it has a low (reportedly 4%) chance of inducing cutaneous reactions among persons who have a history of such reactions to aspirin or non-selective NSAIDs.
Celecoxib is predominantly metabolized by cytochrome P450 2D6. Caution must be exercised with concomitant use of 2D6 inhibitors, such as fluconazole, which can greatly elevate celecoxib serum levels. In addition, celecoxib may antagonize or increase the risk of renal failure with angiotensin converting enzyme-inhibitors, such as lisinopril, and diuretics, such as hydrochlorothiazide.
Celecoxib is labeled as pregnancy category C. It is contraindicated during the third trimester of pregnancy due to teratogenic potential.
Risk of heart attack and stroke
There has been much concern about the possibility of increased risk for heart attack and stroke in users of NSAID drugs, particularly COX-2 selective NSAIDs such as celecoxib, since the withdrawal of the COX-2 inhibitor rofecoxib (Vioxx) in 2004. Like all NSAIDs on the U.S. market, celecoxib carries an FDA-mandated "black box warning" for cardiovascular and gastrointestinal risk. In February 2007, the American Heart Association warned that celecoxib should be used "as a last resort on patients who have heart disease or a risk of developing it", and suggested that paracetamol (acetaminophen), or certain older NSAIDs, such as naproxen, may be safer choices for chronic pain relief in these patients.
The cardiovascular risks of celecoxib are controversial, with apparently contradictory data produced from different clinical trials. In December 2004, "APC", the first of two trials of celecoxib for colon cancer prevention, found that long-term (33 months) use of high-dose Celebrex (400 and 800 mg daily) demonstrated an increased cardiovascular risk compared with placebo. A similar trial, named PreSAP, did not demonstrate an increased risk. Still, the APC trial, combined with the recent Vioxx findings, suggested that there might be serious cardiovascular risks specific to the COX-2 inhibitors. On the other hand, a large Alzheimer's prevention trial, called ADAPT, was terminated early after preliminary data suggested that the nonselective NSAID naproxen, but not celecoxib, was associated with increased cardiovascular risk. In 2005, a study published in the Annals of Internal Medicine found that cardiovascular effects of COX-2 inhibitors differ, depending on the drug. Other COX-2 selective inhibitors, such as rofecoxib, have significantly higher myocardial infarction rates than celecoxib. In April 2005, after an extensive review of data, the FDA concluded that it was likely "that there is a 'class effect' for increased CV risk for all NSAIDs". In a 2006 meta-analysis of randomized control studies, the cerebrovascular events associated with COX-2 inhibitors were examined, but no significant risks were found when compared to non-selective NSAIDs or placebos.
Two studies on the cardiovascular risks of celecoxib and other NSAIDs were meta-analyses, published in 2006. The first of these, published in the British Medical Journal, looked at the incidence of cardiovascular events in all previous randomized controlled trials of COX-2 inhibitors, as well as some trials of other NSAIDs. The authors concluded that a significant increased risk did exist for celecoxib, as well as some other selective and nonselective NSAIDS. However, the increased cardiovascular risk in celecoxib was noted only at daily doses of 400 mg or greater. A second meta-analysis published in the Journal of the American Medical Association, which included observational rather than randomized studies (mostly at lower doses) did not find an increased cardiovascular risk of celecoxib vs placebo.
The Vioxx Gastrointestinal Outcomes Research (VIGOR) trial presented a five-fold increase in atherothrombotic cardiovascular events associated with rofecoxib compared to naproxen. Although, the Celecoxib Long-Term Arthritis Safety Study (CLASS) did not present an increase in occurrence of such events, many experts believe that the risk associated with rofecoxib long-term use also applies to celecoxib based on the pharmacology in three distinct mechanisms. It is suggested that prostacyclin (PGI2) inhibition with relatively unopposed platelet-derived thromboxane (TxA2) generation may lead to thrombotic risks. PGI2 from endothelial cells by COX-2 catalysis has anti-aggregating, anti-proliferative, and vasodilating properties. Conversely, TxA2 from platelets maintain vascular homeostasis by irreversible platelet aggregating, vasoconstricting, and smooth muscle proliferating properties. The imbalance of PGI2 may promote TxA2 thrombosis. In addition, COX-2 selective inhibitors can elevate blood pressure by allowing a normal amount of the vasoconstrictor, TxA2, and a stark decrease in the levels of the vasodilator, PGI2., Furthermore, a third postulate for promoting atherothombotic events includes that the upregulation of COX-2 plays a key role in cardioprotection of the last phase of ischemic preconditioning. Due to the controversy, it is advised that prescribers use caution when prescribing celecoxib and present rational care plans that demonstrate a clear indication for the medication.
To establish more conclusively the true cardiovascular risk profile of celecoxib, Pfizer agreed to fund a large, randomized trial specifically designed for that purpose. The trial, centered at the Cleveland Clinic, with a planned enrollment of 20,000 high-risk patients. Celecoxib will be compared with the non-selective NSAIDS naproxen and ibuprofen. Since all patients have arthritis, ethical considerations make it difficult to have a placebo group. This trial has began enrollment in 2006 according to the Clinical Trials database, and is not scheduled to be completed until May 2014. Ultimately, this trial will help answer the question as to whether Celebrex has a riskier cardiovascular profile compared with naproxen or ibuprofen.
Celecoxib is a highly selective COX-2 inhibitor and primarily inhibits this isoform of cyclooxygenase (and thus causes inhibition of prostaglandin production), whereas nonselective NSAIDs (like asprin, naproxen and ibuprofen) inhibit both COX-1 and COX-2. COX-1, traditionally defined as a constitutively-expressed “housekeeping” enzyme, is the only isoenzyme found in platelets and plays a role in the protection of the gastrointestinal mucosa, renal hemodynamics, and platelet thrombogenesis. COX-2, on the contrary, is extensively expressed in cells involved in inflammation and is upregulated by bacterial lipopolysaccharides, cytokines, growth factors, and tumor promoters. Celecoxib is approximately 10-20 times more selective for COX-2 inhibition over COX-1. It binds with its polar sulfonamide side chain to a hydrophilic side pocket region close to the active COX-2 binding site. In theory, this selectivity allows celecoxib and other COX-2 inhibitors to reduce inflammation (and pain) while minimizing gastrointestinal adverse drug reactions (e.g. stomach ulcers) that are common with non-selective NSAIDs.
Celecoxib inhibits COX-2 without affecting COX-1. COX-1 is involved in synthesis of prostaglandins and thromboxane, but COX-2 is only involved in the synthesis of prostaglandin. Therefore, inhibition of COX-2 inhibits only prostaglandin synthesis without affecting thromboxane (TXA2) and thus offer no cardioprotective effects of non-selective NSAIDs.
The synthesis of celecoxib was first described in 1997 by a team of researchers at Searle Research and Development. Celecoxib is synthesized by a Claisen condensation reaction of an acetophenone with N-(trifluoroacetyl)imidazole catalyzed by the strong base, sodium bis(trimethylsilyl)amide to produce a 1,3-dicarbonyl adduct. Condensation of the diketone with (4-sulfamoylaphenyl)hydrazine produces the 1,5-diarylpyrazole drug moiety.
The Searle research group found that the two appropriately substituted aromatic rings must reside on adjacent positions about the central ring for adequate COX-2 inhibition. Various modifications can be made to the 1,5-diarylpyrazole moiety to deduce the structure-activity relationship of celecoxib. It was found that a para-sulfamoylphenyl at position 1 of the pyrazole has a higher potency for COX-2 selective inhibition than a para-methoxyphenyl (see structures 1 and 2, below). In addition, it is known that a 4-(methylsulfonyl)phenyl or 4-sulfamoylphenyl is necessary for COX-2 inhibition. For instance, replacing either of these entities with a –SO2NHCH3 substituent diminishes COX-2 inhibitory activity as noted with a very high inhibitory concentration-50 (see structures 3 - 5). At the 3-position of the pyrazole, a trifluoromethyl or difluoromethyl provides superior selectivity and potency compared to a fluoromethyl or methyl substitution (see structures 6 – 9).
The fourth position of the pyrazole is readily affected by steric hindrance such that increasing the bulkiness of the substitution starkly decreases the potency. For example, by progressively increasing the size of R1, from a methyl to propyl, the potency for COX-2 inhibition decreases especially with moieties larger than an ethyl (see structures 10-12). In addition, incorporating a halo-atom at this position provides significantly potent COX-2 inhibition (see structures 13 and 14). While it is known that there must be an aromatic system at the fifth position of the pyrazole, optimizing this substituent is difficult since it is not known what combination of modifications will provide the highest potency and selectivity due to the flexible nature of the 5-aryl system. It was found that substitutions at either the para (4-substitution) or ortho (2-substitution) sites have higher potency than meta (3-substitution) sites (see structures 15-17).
Electron withdrawing groups, such as –CN, at these positions have poor COX-1 and COX-2 inhibition; however, electron donating groups, such as methoxyl, have substantial COX-1 and COX-2 inhibitory effects which makes it inefficient as a COX-2 selective inhibitor (see structures 18 and 19 ). The strong COX-1 inhibition of the para-methoxyl can be corrected by substituting a halo-atom at the alpha position. For instance, the introduction of a 3-fluoro or 3-chloro decreases COX-1 inhibition by 43- and 33-folds, respectively (see structures 20 and 21). It is necessary to consider the steric hindrance created by a para-substitution of the 5-aromatic system. Consider the COX-2 inhibitory capacity of the 4-methyl and 4-ethyl modifications: 4-methyl can inhibit COX-2 such that the IC50 is 0.040μM while that of the 4-ethyl is 0.86μM which means that the 4-methyl substituent is at least 20-fold more potent (see structures 22 and 23).
Celecoxib is compound 22; the 4-sulfamoylphenyl on the 1-pyrazol substituent is required for COX-2 inhibition and the 4-methyl on the 5-pyrazol system has low steric hindrance to maximize potency while the 3-trifluoromethyl group provides superior selectivity and potency. To explain the selectivity of celecoxib, it is necessary to analyze the free energy of binding difference between the drug molecule and COX-1 compared to COX-2 enzymes. The structural modifications highlight the importance of binding to residue 523 in the side binding pocket of the cyclooxygenase enzyme, which is an isoleucine in COX-1 and a valine in COX-2. It appears that this mutation contributes to COX-2 selectivity by creating steric hindrance between the sulfonamide oxygen and the methyl group of Ile523 that effectively destabilizes the celecoxib-COX-1 complex. . Thus it is reasonable to expect COX-2 selective inhibitors to be more bulky than non-selective NSAIDs.
Celecoxib was developed by G. D. Searle & Company and co-promoted by Monsanto Company (parent company of Searle) and Pfizer under the brand name Celebrex. Monsanto merged with Pharmacia, from which the Medical Research Division was acquired by Pfizer, giving Pfizer ownership of Celebrex. The drug was at the core of a major patent dispute that was resolved in Searle's favor (later Pfizer) in 2004. In University of Rochester v. G.D. Searle & Co., 358 F.3d 916 (Fed. Cir. 2004), the University of Rochester claimed that United States Pat. No. 6,048,850 (which claimed a method of inhibiting COX-2 in humans using a compound, without actually disclosing what that compound might be) covered drugs such as celecoxib. The court ruled in favor of Searle, holding in essence that the University had claimed a method requiring, yet provided no written description of, a compound that could inhibit COX-2 and therefore the patent was invalid.
After the withdrawal of rofecoxib (Vioxx) from the market in September 2004, Celebrex enjoyed a robust increase in sales. However, the results of the APC trial in December of that year raised concerns that Celebrex might carry risks similar to those of Vioxx, and Pfizer announced a moratorium on direct-to-consumer advertising of Celebrex soon afterwards. After a significant drop, sales of Celebrex have recovered, and reached $2 billion in 2006. Pfizer resumed advertising Celebrex in magazines in 2006, and resumed television advertising in April 2007 with an unorthodox, 2½ minute advertisement which extensively discussed the adverse effects of Celebrex in comparison with other anti-inflammatory drugs. The ad drew criticism from the consumer advocacy group Public Citizen, which called the ad's comparisons misleading. Pfizer has responded to Public Citizen's concerns with assurances that they are truthfully advertising the risk and benefits of Celebrex as set forth by the FDA.
In late 2007, Pfizer released another U.S. television ad for Celebrex, which also discussed celecoxib's adverse effects in comparison with those of other anti-inflammatory drugs.
Dr. Simmons of Brigham Young University, who discovered the COX-2 enzyme, is suing Pfizer to be credited with discovery of the technique in 1989 that eventually led to the drug, and for $1 billion USD. The company has made about $30 billion from the drug as of 2006. 
Research into cancer prevention
The role that celecoxib might have in reducing the rates of certain cancers has been the subject of many studies. However, given the side effects of anti-COX-2 on rates of heart disease, there is no current medical recommendation to use this drug for cancer reduction.
- Colorectal cancer risk is clearly reduced in people regularly taking a NSAID like aspirin or celecoxib. In addition, some epidemiological studies, and most preclinical studies pointed out that specific COX-2 inhibitors like celecoxib are more potent and less toxic than "older" NSAIDs. Twelve carcinogenesis studies support that celecoxib is strikingly potent to prevent intestinal cancer in rats or mice (data available on the Chemoprevention Database). Small-scale clinical trials in very high risk people (belonging to FAP families) also indicate that celecoxib can prevent polyp growth. Hence large-scale randomized clinical trials were undertaken and results published by N. Arber and M. Bertagnolli in the New England Journal of Medicine, August 2006. Results show a 33 to 45% polyp recurrence reduction in people taking 400–800 mg celecoxib each day. However, serious cardiovascular events were significantly more frequent in the celecoxib-treated groups (see above, cardiovascular toxicity). Aspirin shows a similar (and possibly larger) protective effect, has demonstrated cardioprotective effects and is significantly cheaper, but there have been no head-to-head clinical trials comparing the two drugs.
Research into cancer treatment
Different from cancer prevention, cancer treatment is focused on the therapy of tumors that have already formed and have established themselves inside the patient. Many studies are ongoing to determine whether celecoxib might be useful for this latter condition. However, during molecular studies in the laboratory, it became apparent that celecoxib could interact with other intracellular components besides its most famous target, cyclooxygenase 2 (COX-2). The discovery of these additional targets has generated much controversy, and the initial assumption that celecoxib reduces tumor growth primarily via the inhibition of COX-2 became contentious.
Certainly, the inhibition of COX-2 is paramount for the anti-inflammatory and analgesic function of celecoxib. However, whether inhibition of COX-2 also plays a dominant role in this drug’s anticancer effects is unclear. For example, a recent study with malignant tumor cells showed that celecoxib could inhibit the growth of these cells in vitro, but COX-2 played no role in this outcome; even more strikingly, the anticancer effects of celecoxib were also obtained with the use of cancer cell types that don’t even contain COX-2.
Additional support for the idea that other targets besides COX-2 are important for celecoxib's anticancer effects has come from studies with chemically modified versions of celecoxib. Several dozen analogs of celecoxib were generated with small alterations in their chemical structures. Some of these analogs retained COX-2 inhibitory activity, whereas many others didn't. However, when the ability of all these compounds to kill tumor cells in cell culture was investigated, it turned out that the antitumor potency did not at all depend on whether or not the respective compound could inhibit COX-2, showing that inhibition of COX-2 was not required for the anticancer effects. One of these compounds, 2,5-dimethyl-celecoxib, which entirely lacks the ability to inhibit COX-2, actually turned out to display stronger anticancer activity than celecoxib itself.
Research into adhesion prevention
Celocoxib may prevent intra-abdominal adhesion formation. Adhesions are a common complication of surgery, especially abdominal surgery, and major cause of bowel obstruction and infertility. Publishing in 2005, researchers in Boston noticed a "dramatic" reduction in post-surgical adhesions in mice taking the drug celecoxib. Multi-institutional trials in adult human patients are planned. The initially suggested course of treatment is a mere 7–10 days following surgery.
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- ^ Arin K. Greene, MD, MMSc,Ian P. J. Alwayn, MD, PhD, Vania Nose, MD, PhD, Evelyn Flynn, MA, David Sampson, BA, David Zurakowski, PhD, Judah Folkman, MD, and Mark Puder, MD (July 2005). "Prevention of Intra-abdominal Adhesions Using the Antiangiogenic COX-2 Inhibitor Celecoxib". Ann Surg. 242 (1): 140–146. doi:10.1097/01.sla.0000167847.53159.c1. PMC 1357715. PMID 15973112. http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=1357715.
- ^ "Celebrex Prevents Adhesions After Surgery". Children's Hospital Boston. January 26, 2005. http://www.childrenshospital.org/newsroom/Site1339/mainpageS1339P1sublevel119.html. Retrieved 2009-03-11.
- ^ Viinikka, Tai (February 25, 2005). "COX-2 Inhibitors May Prevent Common Surgical Complication". Focus Online. Harvard Medical, Dental, and Public Health Schools. http://focus.hms.harvard.edu/2005/Feb25_2005/research_briefs.html. Retrieved 2009-03-11.
- Celebrex website run by Pfizer
- FDA Alert for Practitioners on Celebrex (celecoxib), published December 17, 2004
- FDA Alert for Healthcare Professionals published July 4, 2005
- Largest systematic review of adverse renal and arrhythmia risk of Celecoxib and other COX-2 inhibitors, in JAMA 2006
- U.S. National Library of Medicine: Drug Information Portal - Celecoxib
Intracellular chemotherapeutic agents/antineoplastic agents (L01) SPs/MIs
(M phase)Block microtubule assemblyBlock microtubule disassembly
inhibitorIIICrosslinking of DNA
(CCNS)Aziridines: Carboquone • ThioTEPA • Triaziquone • Triethylenemelamine
Photosensitizers/PDT OtherOther/ungroupedAmsacrine • Trabectedin • retinoids (Alitretinoin, Tretinoin) • Arsenic trioxide • asparagine depleters (Asparaginase/Pegaspargase) • Celecoxib • Demecolcine • Elesclomol • Elsamitrucin • Etoglucid • Lonidamine • HAMLET (human alpha-lactalbumin made lethal to tumor cells) • Lucanthone • Mitoguazone • Mitotane • Oblimersen • Omacetaxine mepesuccinate • mTOR inhibitors (Everolimus, Temsirolimus)
tumr, epon, para
Anti-inflammatory products (M01A) Pyrazolidine/Butylpyrazolidines Acetic acid derivatives
and related substances
Oxicams Propionic acid derivatives Fenamates Coxibs Other Non-steroidal anti-inflammatory drug (NSAID) products (primarily M01A and M02A, also N02BA) Salicylates Arylalkanoic acids 2-Arylpropionic acids
Pyrazolidine derivatives Oxicams COX-2 inhibitors Sulfonanilides Topically used products COX-inhibiting nitric oxide donators Others Analgesics (N02A, N02B) Opioids
See also: Opioids templateOpium & alkaloids thereofSemi-synthetic opium
Pyrazolones Cannabinoids Anilides Non-steroidal
See also: NSAIDs templatePropionic acid classOxicam classAcetic acid classAnthranilic acid
Meclofenamate • Mefenamic acidSalicylates
Atypical, adjuvant and potentiators,
Metabolic agents and miscellaneousAmitryptiline • Befiradol • Bicifadine • Carisoprodol • Camphor • Cimetidine • Clonidine • Chlorzoxazone • Cyclobenzaprine • Duloxetine • Esreboxetine • Flupirtine • Gabapentin • Glafenine • Hydroxyzine • Ketamine • Menthol • Mephenoxalone • Methocarbamol • Nefopam • Orphenadrine • Pregabalin • Proglumide • Scopolamine • Tebanicline • Trazodone • Gabapentin enacarbil • Ziconotide
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Celecoxib — Nombre (IUPAC) sistemático 4 [5 (4 metilfenil) 3 (trifluorometil) pirazol 1 il]benzeno sulfonamida … Wikipedia Español
Celecoxib — Célécoxib Célécoxib Général No CAS … Wikipédia en Français
Célécoxib — Général No CAS … Wikipédia en Français
celecoxib — fármaco anti inflamatorio no esteroídico inhibidor selectivo de la ciclooxigenasa 2 (COX 2) Diccionario ilustrado de Términos Médicos.. Alvaro Galiano. 2010 … Diccionario médico
Celecoxib — Strukturformel Allgemeines Freiname Celecoxib … Deutsch Wikipedia
celecoxib — A drug that reduces pain. Celecoxib belongs to the family of drugs called nonsteroidal anti inflammatory agents. It is being studied in the prevention of cancer … English dictionary of cancer terms
celecoxib — noun a Cox 2 inhibitor (trade name Celebrex) that relieves pain and inflammation without harming the digestive tract • Syn: ↑Celebrex • Usage Domain: ↑trade name (for: ↑Celebrex) • Hypernyms: ↑Cox 2 inhibitor … Useful english dictionary
celecoxib — noun A non steroidal anti inflammatory drug used in the treatment of osteoarthritis, rheumatoid arthritis, acute pain, painful menstruation and menstrual symptoms, and to reduce numbers of colon and rectum polyps in patients with familial… … Wiktionary
celecoxib — cel·e·cox·ib .sel ə käk sib n an NSAID C17H14F3N3O2S that is a COX 2 inhibitor administered orally esp. to relieve the pain and inflammation of osteoarthritis and rheumatoid arthritis see celebrex * * * n. an anti inflammatory drug (see NSAID)… … Medical dictionary
celecoxib — n. an anti inflammatory drug (see NSAID) that selectively inhibits cyclo oxygenase 2 (see COX 2 inhibitor). It is taken by mouth in the treatment of osteoarthritis and rheumatoid arthritis. Trade names: Celebrex … The new mediacal dictionary