COX-2 (IC50 = 40 nM); COX-1 (IC50 = 15 μM); non-steroidal anti-inflammatory drug (NSAID)

Celecoxib (10-75 μM), a selective cyclooxygenase-2 (COX-2) inhibitor, suppresses nasopharyngeal cancer cell line proliferation in a dose-dependent manner. In NPC cell lines, celecoxib (25 and 50 μM) caused apoptosis and cell cycle arrest at the G0/G1 checkpoint, which was linked to a notable reduction in STAT3 phosphorylation. Genes downstream of STAT3, including Survivin, Mcl-1, Bcl-2, and Cyclin D1, were markedly downregulated following exposure to Celecoxib (25 and 50 μM) [2]. Celecoxib, which targets the transcriptional target cyclooxygenase 2 (COX-2), reduces the growth and carcinogenesis of NF2 mutant cells [6]. Combining TTNPB (3 μM) with celecoxib (5 μM, 28 days) causes fibroblasts to become articular chondrocytes [7]. Mesenchymal cells generated from Wharton's jelly are encouraged to transdifferentiate into endothelial progenitor cells by celecoxib (10 μM, 7–14 days) [8]. Human aortic valve interstitial cells undergo transdifferentiation into myofibroblasts when exposed to celecoxib (5 μM) for 14 days [9].

Oral celecoxib exhibits strong anti-inflammatory properties. In an adjuvanted arthritis model, celecoxib reduces chronic inflammation with an ED50 of 0.37 mg/kg/day, and it reduces acute inflammation in the carrageenan edema test with an ED50 of 7.1 mg/kg. With an ED50 of 34.5 mg/kg, celecoxib additionally demonstrated analgesic efficacy in the Hargreaves hyperalgesia model. Despite being just as effective as conventional NSAIDs, celecoxib did not cause acute gastrointestinal toxicity in rats when administered at doses as high as 200 mg/kg. Furthermore, no chronic gastrointestinal damage was observed in rats even dosages as high as 600 mg/kg/day for 10 days [1]. Tumor weight was 66% lower in KpB mice given an obese, high-fat diet when treated with celecoxib than in control animals. Celecoxib treatment reduced tumor weight by 46% in KpB mice fed a low-fat (non-obesogenic) diet [3]. For two weeks, either an intramuscular injection of Fasudil (10 mg/kg) or oral Celecoxib (20 mg/kg) was given to the rat model. The findings demonstrate that in rats with spinal cord injury, the combination of celecoxib and facudil can dramatically reduce the expression of COX-2 and Rho kinase II surrounding the lesion site, improve the pathological morphology of the injured spinal cord, and aid in the promotion of motor function recovery [4].

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The objective was to evaluate the effect of the COX-2 inhibitor, celecoxib, on (1) proliferation and apoptosis in human ovarian cancer cell lines and primary cultures of ovarian cancer cells, and (2) inhibition of tumor growth in a genetically engineered mouse model of serous ovarian cancer under obese and non-obese conditions. Celecoxib inhibited cell proliferation in three ovarian cancer cell lines and five primary cultures of human ovarian cancer after 72 hours of exposure. Treatment with celecoxib resulted in G1 cell cycle arrest, induction of apoptosis, inhibition of cellular adhesion and invasion and reduction of expression of hTERT mRNA and COX-2 protein in all of the ovarian cancer cell lines. In the KpB mice fed a high fat diet (obese) and treated with celecoxib, tumor weight decreased by 66% when compared with control animals. Among KpB mice fed a low fat diet (non-obese), tumor weight decreased by 46% after treatment with celecoxib. In the ovarian tumors from obese and non-obese KpB mice, treatment with celecoxib as compared to control resulted in decreased proliferation, increased apoptosis and reduced COX-2 and MMP9 protein expression, as assessed by immunohistochemistry. Celecoxib strongly decreased the serum level of VEGF and blood vessel density in the tumors from the KpB ovarian cancer mouse model under obese and non-obese conditions. This work suggests that celecoxib may be a novel chemotherapeutic agent for ovarian cancer prevention and treatment and be potentially beneficial in both obese and non-obese women[3].

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Resistance mechanisms of rho-associated kinase (ROCK) inhibitors are associated with the enhanced expression of cyclooxygenase-2 (COX-2). The therapeutic effects of ROCK on nervous system diseases might be enhanced by COX-2 inhibitors. This study investigated the synergistic effect of the combined use of the ROCK inhibitor fasudil and a COX-2 inhibitor celecoxib on spinal cord injury in a rat model established by transecting the right half of the spinal cord at T11. Rat models were orally administrated with celecoxib (20 mg/kg) and/or intramuscularly with fasudil (10 mg/kg) for 2 weeks. Results demonstrated that the combined use of celecoxib and fasudil significantly decreased COX-2 and Rho kinase II expression surrounding the lesion site in rats with spinal cord injury, improved the pathomorphology of the injured spinal cord, and promoted the recovery of motor function. Moreover, the effects of the drug combination were better than celecoxib or fasudil alone. This study demonstrated that the combined use of fasudil and celecoxib synergistically enhanced the functional recovery of injured spinal cord in rats.[4]

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Nonalcoholic fatty liver disease (NAFLD) is a kind of liver lipid synthesis and degradation imbalance related with metabolic syndrome. Celecoxib shows the function of ameliorating NAFLD, but the underlying mechanisms remain unknown. Here, we discuss the possible mechanisms of celecoxib alleviating NAFLD by restoring autophagic flux. Lipids were accumulated in L02 cells treated with palmitate as well as SD rats fed with high-fat diet. Western blot showed that LC3 II/I was higher and p62 was lower on the early stage of steatosis while on the late stage both of them were higher, indicating that autophagic flux was activated on the early stage of steatosis, but blocked on the late stage. Rapamycin alleviated steatosis with activating autophagic flux while chloroquine aggravated steatosis with inhibiting autophagic flux. COX-2 siRNA and celecoxib were used to inhibit COX-2. Western blot and RFP-GFP-LC3 double fluorescence system indicated that celecoxib could ameliorate steatosis and restore autophagic flux in L02 cells treated with palmitate as well as SD rats fed with high-fat diet. In conclusion, celecoxib partially restores autophagic flux via downregulation of COX-2 and alleviates steatosis in vitro and in vivo [5].

Biological Methods. [1]
Expression and purification of recombinant human COX-1 and COX-2 enzymes, in vitro COX-1 and COX-2 enzyme assays, and the rat gastric toxicity studies have been described previously.

Aim: To investigate the mechanisms underlying the anticancer effect of celecoxib on nasopharyngeal carcinoma (NPC).
Methods: NPC cell lines, HNE1 and CNE1-LMP1, were treated with various concentrations of celecoxib for 48 h. The antiproliferative effect of celecoxib was assessed using MTT assay. Both cell cycle profiles and apoptosis were analyzed using flow cytometry. Western blot was used to measure the levels of signal transducer and activator of transcription 3 (STAT3), phosphorylated STAT3(Y705) (pSTAT3(Y705)), COX-2, Survivin, Mcl-1, Bcl-2 and Cyclin D1.
Results: Celecoxib (10-75 μmol/L) inhibited the proliferation of the NPC cell lines in a dose-dependent manner. Celecoxib (25 and 50 μmol/L) induced apoptosis and cell-cycle arrest at the G(0)/G(1) checkpoint in the NPC cell lines, which was associated with significantly reduced STAT3 phosphorylation. The genes downstream of STAT3 (ie, Survivin, Mcl-1, Bcl-2 and Cyclin D1) were significantly down-regulated after exposure to celecoxib (25 and 50 μmol/L).
Conclusion: The anticancer effects of celecoxib on NPC cell lines results from inducing apoptosis and cell cycle arrest, which may be partly mediated through the STAT3 pathway [2].

Rat Carrageenan-Induced Foot Pad Edema Assay.[1]
Male Sprague−Dawley rats (195−250 g) were fasted with free access to water at least 16 h prior to experiments. The rats were dosed orally with a 1 mL suspension of test compound (Celecoxib) in vehicle (0.5% methyl cellulose and 0.025% Tween-20) or with vehicle alone. One hour later a subplantar injection of 0.1 mL of a 1% solution of carrageenan in 0.9% sterile saline was administered to the right hind foot pad. Paw volume was measured with a displacement plethysmometer 3 h after carrageenan injection.

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Rat Carrageenan-Induced Hyperalgesia Assay.[1]
Male Sprague−Dawley rats were treated as described above. Three hours after carrageenan injection, the rats were placed in a Plexiglass container with a transparent floor with a high intensity lamp heat source positioned under it. After an initial 20 min period, thermal stimulation was begun on either the injected foot or the contralateral uninjected foot. A photoelectric cell turned off the lamp and timer when light was interrupted by paw withdrawal. The withdrawal latency period in seconds was determined for the control and drug-treated groups, and percent inhibition of the stimulus-induced decrease in withdrawal latency was determined.

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Rat Adjuvant-Induced Arthritis Assay.[1]
Arthritis was induced in male Lewis rats (125−150 g) by injection of 1 mg of Mycobacterium butyricum in 50 μL of mineral oil into the right hind foot pad. Fourteen days after injection of adjuvant, the contralateral left foot volume was measured with a displacement plethysmometer. Animals with paw volumes 0.37 mL greater than normal paws were then randomized and treated with test compound/Celecoxib (as a suspension in 0.5% methyl cellulose and 0.025% Tween-20), beginning on day 15 postadjuvant injection. Animals were dosed twice daily by gavage at the indicated doses with a volume of 1.0 mL/day. Compound administration was continued until final assessment on day 25 postadjuvant injection, and the mean inhibition was determined on the basis of an average of 8−10 animals. The typical increase in contralateral paw volume measured on day 25 was 1.4−1.9 mL.

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Dissolved in 0.5% methyl cellulose and 0.025% Tween-20; ≤200 mg/kg; p.o. administration

A 0.1 mL aliquot of a 1% solution of carrageenan in 0.9% sterile saline or 1 mg of Mycobacterium butyricum in 50 μL of mineral oil is administered to the right hind foot pad of male Sprague Dawley rats.

Absorption, Distribution and Excretion
Celecoxib is absorbed rapidly in the gastrointestinal tract. When a single oral dose of 200 mg was given to healthy research subjects, the peak plasma levels of celecoxib occurred within 3 hours. The Cmax is 705 ng/mL. When multiple doses are given, steady-state concentrations are reached on or before day 5. When taken with a high-fat meal, peak plasma levels are delayed for about 1 to 2 hours with an increase in total absorption (AUC) of 10% to 20%. The AUC of celecoxib has been shown to be significantly lower in patients with chronic renal impairment. A meta-analysis of pharmacokinetic studies has suggested an approximately 40% higher AUC (area under the curve) of celecoxib in black patients compared to Caucasians for unknown reasons.
Celecoxib is primarily eliminated by hepatic metabolism with small amounts (<3%) of the unchanged drug found in both the urine and feces. About 57% of an oral dose of celecoxib is excreted in the feces and 27% is found to be excreted into the urine in the form of metabolites. The main metabolite in urine and feces is identified as the carboxylic acid metabolite (73%). The amount of glucuronide in the urine is reported to be low.
The apparent volume of distribution of celecoxib at steady state (Vss/F) is about 429 L, which suggests wide distribution into various tissues. Celecoxib is not preferentially bound to red blood cells. Another resource reports a volume of distribution of 455 ± 166L.
Apparent clearance (CL/F), single oral 200 mg dose, healthy subjects = 27.7 L/hr. Clearance may be decreased by about 47% in patients with chronic renal insufficiency, according to a pharmacokinetic study. Studies have not been performed in patients with severe renal impairment.
/MILK/ Limited data from 3 published reports that included a total of 12 breastfeeding women showed low levels of Celebrex in breast milk. The calculated average daily infant dose was 10-40 ug/kg/day, less than 1% of the weight-based therapeutic dose for a two-year old-child.
/MILK/ The aim of this study was to investigate the transfer of celecoxib into human milk. In one group of 3 breastfeeding patients on celecoxib at steady state, milk levels were determined at set intervals over 24 hours. Plasma levels were determined in 2 of their infants, age 17 and 22 months. In a second group of 2 subjects, intravenous lines were placed and a single 200-mg dose of celecoxib was followed by multiple paired plasma and milk samples over 8 hours. The mean milk-to-plasma ratio for celecoxib was 0.23 (95% confidence interval [CI]: 0.15-0.31). The average concentration of celecoxib in milk during the 8-hour dosing interval was 66 ug/L (95% CI: 41-89). The absolute infant dose averaged 9.8 ug/kg/d (95% CI: 6.2-13.4); the mean relative infant dose was 0.30%. Therefore, the average clinical dose transferred to the infant daily would be approximately 0.3% of the weight-adjusted maternal dose. ...
/MILK/ A 40 year old woman who was breastfeeding her 5 month old daughter was admitted to the hospital for surgery. In the postoperative period, she received four doses of celecoxib (100 mg twice/day) in addition to other medications. Starting about 5 hours after her last dose, four milk samples were obtained by hand expression over a 24 hour interval. The elimination half life range was 4.0-6.5 hours. These data suggest that celecoxib would be eliminated from breast milk about 24 hours after the last dose. Although maternal plasma was not obtained, the estimated milk:plasma ratios (based on reported adult plasma levels) were 0.27-0.59. the infant did not resume breastfeeding until 48 hours after the last dose. If she had nursed, the estimated maximum infant dose would have have been about 40 ug/kg/day.
/MILK/ /The aim of this study was/ to determine the milk-to-plasma (M/P) concentration ratio of celecoxib, and estimate likely infant exposure. Blood and milk were sampled for 48 hr after oral administration of celecoxib 200 mg to six lactating volunteers. The M/P ratio was derived from the area under the concentration-time curves (0-infinity) and the infant 'dose' estimated from celecoxib concentrations in milk. The median (range) M/P ratio was 0.18 (0.15-0.26). The median (range) infant 'dose' was 0.23% (0.17-0.30%) of the maternal dose, adjusted for weight. ...
For more Absorption, Distribution and Excretion (Complete) data for Celecoxib (11 total), please visit the HSDB record page.

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Metabolism / Metabolites
A large part of celecoxib metabolism is mediated by cytochrome P450 2C9 in the liver with some contribution from CYP3A4 and CYP2C8 and possible contributions from CYP2D6. It is metabolized by biotransformation to carboxylic acid and glucuronide metabolites. Three metabolites, a primary alcohol, a carboxylic acid, and a glucuronide conjugate, have been found in human plasma after celecoxib administration. These are considered inactive metabolites in regards to COX enzyme inhibition. Patients who are known or suspected to have decreased cytochrome P450 2C9 activity or function, based on their previous history, should be administered celecoxib with caution as they may have abnormally high serum concentrations resulting from decreased metabolism celecoxib.
Celecoxib metabolism is primarily mediated via CYP2C9. Three metabolites, a primary alcohol, the corresponding carboxylic acid and its glucuronide conjugate, have been identified in human plasma. These metabolites are inactive as COX-1 or COX-2 inhibitors.
Celecoxib has known human metabolites that include Hydroxy celecoxib.
Hepatic. Celecoxib metabolism is primarily mediated via cytochrome P450 2C9. Three metabolites, a primary alcohol, the corresponding carboxylic acid and its glucuronide conjugate, have been identified in human plasma. CYP3A4 is also involved in the hydroxylation of celecoxib but to a lesser extent. These metabolites are inactive as COX-1 or COX-2 inhibitors.
Route of Elimination: Celecoxib is eliminated predominantly by hepatic metabolism with little (<3%) unchanged drug recovered in the urine and feces. 57% of the oral dose is excreted in the feces and 27% is excreted into the urine. The primary metabolite in urine and feces was the carboxylic acid metabolite (73%). The amount of glucuronide in the urine is low.
Half Life: The effective half-life is approximately 11 hours when a single 200 mg dose is given to healthy subjects. Terminal half-life is generally variable because of the low solubility of the drug thus prolonging absorption.

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Biological Half-Life
The effective half-life of celecoxib is approximately 11 hours when a single 200 mg dose is given to healthy subjects. The terminal half-life of celecoxib varies because of its low solubility, which prolongs absorption.
A 40 year old woman who was breastfeeding her 5 month old daughter was admitted to the hospital for surgery. In the postoperative period, she received four doses of celecoxib (100 mg twice/day) in addition to other medications. Starting about 5 hours after her last dose, four milk samples were obtained by hand expression over a 24 hour interval. The elimination half life range was 4.0-6.5 hours. ...
The plasma elimination half-life of celecoxib following oral administration of a single 200-mg dose under fasting conditions is about 11 hours, and the apparent plasma clearance of the drug is about 500 mL/minute; these parameters exhibit wide intraindividual variability, presumably because the low aqueous solubility of celecoxib prolongs absorption. The half-life of celecoxib is prolonged in patients with renal or hepatic impairment and has been reported to be 13.1 hours in patients with chronic renal insufficiency and 11 or 13.1 hours in patients with mild or moderate hepatic impairment, respectively.

Toxicity Summary
IDENTIFICATION AND USE: Celecoxib is a pale yellow solid. It is a cyclooxygenase-2 (COX-2) inhibitor used in the management of osteoarthritis, rheumatoid arthritis, juvenile rheumatoid arthritis, pain, ankylosing spondylitis, and dysmenorrhea. HUMAN STUDIES: Nonsteroidal anti-inflammatory drugs (NSAIDs) cause an increased risk of serious gastrointestinal (GI) adverse events including bleeding, ulceration, and perforation of the stomach or intestines, which can be fatal. These events can occur at any time during use and without warning symptoms. Elderly patients and patients with a prior history of peptic ulcer disease and/or GI bleeding are at greater risk for serious GI events. Allergic reactions, aggravated allergy, bronchospasm, or generalized or facial edema has been reported in 0.1-1.9% of patients receiving celecoxib. Anaphylactoid reactions and angioedema have occurred in patients receiving celecoxib. As with other NSAIDs, anaphylactic reactions have been reported rarely in patients with no previous exposure to the drug. Erythema multiforme, exfoliative dermatitis, Sweet's syndrome, Stevens-Johnson syndrome, and toxic epidermal necrolysis have been reported rarely in patients receiving celecoxib. Hepatitis, jaundice, or liver failure has been reported in patients receiving celecoxib during postmarketing surveillance. Celecoxib may cause premature closure of the ductus arteriosus. ANIMAL STUDIES: Celecoxib was not carcinogenic in rats given oral doses up to 200 mg/kg for males and 10 mg/kg for females, or in mice given oral doses up to 25 mg/kg for males and 50 mg/kg for females for two years. An increased incidence of fetuses with ventricular septal defects, sternebral fusion, rib fusion, and sternebrae abnormality was observed in reproduction studies in rabbits receiving oral celecoxib dosages of 150 mg/kg daily or more throughout organogenesis. A dose-dependent increase in diaphragmatic hernias was observed in rats receiving oral celecoxib dosages of 30 mg/kg or more daily throughout organogenesis. Celecoxib had no effect on male or female fertility or male reproductive function in rats at oral doses up to 600 mg/kg/day. Celecoxib was not mutagenic in an Ames test and a mutation assay in Chinese hamster ovary (CHO) cells, nor clastogenic in a chromosome aberration assay in CHO cells and an in vivo micronucleus test in rat bone marrow.
The mechanism of action of celecoxib is believed to be due to inhibition of prostaglandin synthesis. Unlike most NSAIDs, which inhibit both types of cyclooxygenases (COX-1 and COX-2), celecoxib is a selective noncompetitive inhibitor of cyclooxygenase-2 (COX-2) enzyme. It binds with its polar sulfonamide side chain to a hydrophilic side pocket region close to the active COX-2 binding site. Both COX-1 and COX-2 catalyze the conversion of arachidonic acid to prostaglandin (PG) H2, the precursor of PGs and thromboxane.

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Interactions
Table: Clinically Significant Drug Interactions with Celecoxib [Table#6655]

[1]. Synthesis and biological evaluation of the 1,5-diarylpyrazole class of cyclooxygenase-2 inhibitors: identification of 4-[5-(4-methylphenyl)-3-(trifluoromethyl)-1H-pyrazol-1-yl]benze nesulfonamide (SC-58635, celecoxib). J Med Chem. 1997. Apr 25;40(9):1347-65.

[2]. Celecoxib induces apoptosis and cell-cycle arrest in nasopharyngeal carcinoma cell lines via inhibition of STAT3 phosphorylation. Acta Pharmacol Sin. 2012 May;33(5):682-90.

[3]. The effect of celecoxib on tumor growth in ovarian cancer cells and a genetically engineered mouse model of serous ovarian cancer. Oncotarget. 2016 Jun 28;7(26):39582-39594.

[4]. Combination of fasudil and celecoxib promotes the recovery of injured spinal cord in rats better than celecoxib or fasudil alone. Neural Regen Res. 2015 Nov;10(11):1836-40.

[5]. Celecoxib alleviates nonalcoholic fatty liver disease by restoring autophagic flux. Sci Rep. 2018 Mar 7;8(1):4108.

[6]. A combat with the YAP/TAZ-TEAD oncoproteins for cancer therapy. Theranostics. 2020 Feb 18;10(8):3622-3635.

Therapeutic Uses
Cyclooxygenase 2 Inhibitors
/CLINICAL TRIALS/ ClinicalTrials.gov is a registry and results database of publicly and privately supported clinical studies of human participants conducted around the world. The Web site is maintained by the National Library of Medicine (NLM) and the National Institutes of Health (NIH). Each ClinicalTrials.gov record presents summary information about a study protocol and includes the following: Disease or condition; Intervention (for example, the medical product, behavior, or procedure being studied); Title, description, and design of the study; Requirements for participation (eligibility criteria); Locations where the study is being conducted; Contact information for the study locations; and Links to relevant information on other health Web sites, such as NLM's MedlinePlus for patient health information and PubMed for citations and abstracts for scholarly articles in the field of medicine. Celecoxib is included in the database.
/Celebrex is indicated/ for the management of the signs and symptoms of osteoarthritis. /Included in US product labeling/
/Celebrex is indicated/ for the management of the signs and symptoms of rheumatoid arthritis. /Included in US product labeling/
For more Therapeutic Uses (Complete) data for Celecoxib (14 total), please visit the HSDB record page.

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Drug Warnings
/BOXED WARNING/ WARNING: RISK OF SERIOUS CARDIOVASCULAR EVENTS. Cardiovascular Thrombotic Events: Nonsteroidal anti-inflammatory drugs (NSAIDs) cause an increased risk of serious cardiovascular thrombotic events, including myocardial infarction, and stroke, which can be fatal. This risk may occur early in the treatment and may increase with duration of use. Celebrex is contraindicated in the setting of coronary artery bypass graft (CABG) surgery.
/BOXED WARNING/ WARNING: RISK OF SERIOUS GASTROINTESTINAL EVENTS. Gastrointestinal Bleeding, Ulceration, and Perforation: Nonsteroidal anti-inflammatory drugs (NSAIDs) cause an increased risk of serious gastrointestinal (GI) adverse events including bleeding, ulceration, and perforation of the stomach or intestines, which can be fatal. These events can occur at any time during use and without warning symptoms. Elderly patients and patients with a prior history of peptic ulcer disease and/or GI bleeding are at greater risk for serious GI events.
A subpopulation of patients with asthma may have aspirin-sensitive asthma which may include chronic rhinosinusitis complicated by nasal polyps; severe, potentially fatal bronchospasm; and/or intolerance to aspirin and other nonsteroidal anti-inflammatory drugs (NSAIDs). Because cross-reactivity between aspirin and other NSAIDs has been reported in such aspirin-sensitive patients, celebrex is contraindicated in patients with this form of aspirin sensitivity. When celebrex is used in patients with preexisting asthma (without known aspirin sensitivity), monitor patients for changes in the signs and symptoms of asthma.
Celebrex is contraindicated in patients with previous serious skin reactions to nonsteroidal anti-inflammatory drugs (NSAIDs).
For more Drug Warnings (Complete) data for Celecoxib (33 total), please visit the HSDB record page.

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Pharmacodynamics
Celecoxib inhibits cyclooxygenase 2 (COX-2) enzyme, reducing pain and inflammation. It is important to note that though the risk of bleeding with celecoxib is lower than with certain other NSAIDS, it exists nonetheless and caution must be observed when it is administered to those with a high risk of gastrointestinal bleeding. **A note on the risk of cardiovascular events** Significant concerns regarding the safety of COX-2 selective NSAIDs emerged in the early 2000s. [Rofecoxib], another member of the COX-2 inhibitor drug class, also known as Vioxx, was withdrawn from the market due to prothrombotic cardiovascular risks. Following an FDA Advisory Committee meeting in 2005, in which data from large clinical outcome trials were evaluated, the FDA concluded that the risk for cardiovascular thrombotic events for both COX-2 selective NSAIDs and nonselective NSAIDs was evident. It was determined that the benefits of celecoxib treatment, however, outweighed the risks. Postmarketing cardiovascular outcomes trial (PRECISION) revealed that the lowest possible dose of celecoxib was similar in cardiovascular safety to moderate strength doses of both naproxen and ibuprofen. Patients who had previous cardiovascular events including acute MI, coronary revascularization, or coronary stent insertion were not evaluated in the trial. It is not advisable to administer NSAIDS to these groups of patients.

C17H14F3N3O2S

381.37

381.075

C, 53.54; H, 3.70; F, 14.94; N, 11.02; O, 8.39; S, 8.41

169590-42-5

Celecoxib;169590-42-5;Celecoxib;169590-42-5

2662

White to off-white solid powder

1.4±0.1 g/cm3

529.0±60.0 °C at 760 mmHg

157-159ºC

273.7±32.9 °C

0.0±1.4 mmHg at 25°C

1.606

4.21

1

7

3

26

577

0

RZEKVGVHFLEQIL-UHFFFAOYSA-N

InChI=1S/C17H14F3N3O2S/c1-11-2-4-12(5-3-11)15-10-16(17(18,19)20)22-23(15)13-6-8-14(9-7-13)26(21,24)25/h2-10H,1H3,(H2,21,24,25)

4-[5-(4-methylphenyl)-3-(trifluoromethyl)pyrazol-1-yl]benzenesulfonamide

SC 58635; YM177. Celecoxib; SC58635; YM-177; 169590-42-5; Celebrex; Celebra; Onsenal; Celecox; Celocoxib; 184007-95-2; SC-58635; YM 177; trade name Celebrex; Xilebao.

2934.99.9001

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)