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Rofecoxib (MK 966)

Alias: MK-0966; MK0966; MK0966; MK966; MK966; MK 966; MK 0966; Trade name: Vioxx; Ceoxx; Ceeoxx.
Cat No.:V1045 Purity: ≥98%
Rofecoxib (formerly MK-0966; MK0966; MK-966; MK966; Vioxx; Ceoxx; Ceeoxx.), an NSAID drug, is a potent and selective COX-2 inhibitor with potential anti-inflammatory activity.
Rofecoxib (MK 966)
Rofecoxib (MK 966) Chemical Structure CAS No.: 162011-90-7
Product category: COX
This product is for research use only, not for human use. We do not sell to patients.
Size Price Stock Qty
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500mg
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Other Forms of Rofecoxib (MK 966):

  • Rofecoxib-d5 (rofecoxib d5)
Official Supplier of:
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Purity & Quality Control Documentation

Purity: ≥98%

Product Description

Rofecoxib (formerly MK-0966; MK0966; MK-966; MK966; Vioxx; Ceoxx; Ceeoxx.), an NSAID drug, is a potent and selective COX-2 inhibitor with potential anti-inflammatory activity. It inhibits COX-2 with an IC50 of 18 NM. Rofecoxib belongs to the nonsteroidal anti-inflammatory drug (NSAID) class and has now been withdrawn from the market due to safety concerns. Rofecoxib exhibits anti-inflammatory, analgesic, and antipyretic activities in animal models. The mechanism of action of rofecoxib is believed to be due to inhibition of prostaglandin synthesis, via inhibition of cyclooxygenase-2 (COX-2).

Biological Activity I Assay Protocols (From Reference)
ln Vitro
In human osteosarcoma cells and Chinese hamster ovary cells, rofecoxib (MK-0966) has IC50s of 26 and 18 nM for human COX-2, respectively. It has a 1000-fold selectivity for COX-2 over COX-1 (IC50 >50 μM in U937 cells and >15 μM in Chinese hamster ovary cells). Rofecoxib is a strong and oral active inhibitor of COX-2. Rofecoxib suppresses purified human COX-1 in a non-time-dependent way that is only visible at extremely low substrate concentrations (IC50=26 μM at 0.1 μM arachidonic acid concentration), whereas it time-dependently inhibits purified human recombinant COX-2 (IC50=0.34 μM). When it comes to the suppression of COX-1-derived thromboxane B(2) synthesis after blood coagulation, rofecoxib has a higher IC50 value of 18.8 ± 0.9 μM than lipopolysaccharide-induced, COX-2-derived PGE(2) synthesis [1]. Cell proliferation is induced by ropecoxib (36 μM) at 68% in MPP89, 58% in Ist-Mes-1, and 40% in Ist-Mes-2. The survival rates of MSTO-211H and NCI-H2452 after receiving 36 μM of rofecoxib are 97% and 90%, respectively. In Ist-Mes-1, Ist-Mes-2, and MPP89 cell lines, ropecoxib (36 μM) reduces the levels of COX-2 and mRNA[3].
ln Vivo
In mouse models, rofecoxib potently suppresses the following: lipopolysaccharide-induced pyresis (ID50=0.24 mg/kg), carrageenan-induced paw edema (ID50=1.5 mg/kg), and adjuvant-induced arthritis (ID50=0.74 mg/kg/day). In rats, rofecoxib also prevents the degradation of bone and cartilage caused by adjuvants. Ropecoxib has no effect at doses up to 200 mg/kg/day for five days in a 51Cr excretion experiment used to assess gastrointestinal integrity in either rats or squirrel monkeys[1]. In mice, the blood vessels connected to the internal limiting membrane (ILM) are diminished by rofecoxib (15 mg/kg, ip). In ROP mice, Rofecoxib also greatly reduces the expressions of the COX-2 and VEGF proteins, as well as the COX-2 and VEGF mRNAs[2].
Animal Protocol
Dissolved in 80% PEG 200 in distilled water; 0.1, 0.3, 1.0, and 3.0 mg/kg/day; p.o. administration
Rat adjuvant-induced arthritis (AIA) model
ADME/Pharmacokinetics
Absorption, Distribution and Excretion
The mean oral bioavailability of rofecoxib at therapeutically recommended doses of 12.5, 25, and 50 mg is approximately 93%.
Approximately 72% and 14% of a radioactive rofecoxib dose is eliminated in the urine as metabolites and /in/ feces as unchanged drug, respectively.
Time to peak concentration: Approximately 2 to 3 hours.
At steady state, the apparent volume of distribution is about 91 and 86 L after a 12.5 and 25 mg dose, respectively.
At recommended doses, the mean oral bioavailability is 93%. The peak plasma concentration and area under the plasma concentration-time curve are roughly proportional across the clinical dose range.
For more Absorption, Distribution and Excretion (Complete) data for ROFECOXIB (11 total), please visit the HSDB record page.
Metabolism / Metabolites
Hepatic. Metabolism of rofecoxib is primarily mediated through reduction by cytosolic enzymes. The principal metabolic products are the cis-dihydro and trans-dihydro derivatives of rofecoxib, which account for nearly 56% of recovered radioactivity in the urine. An additional 8.8% of the dose was recovered as the glucuronide of the hydroxy derivative, a product of oxidative metabolism. The biotransformation of rofecoxib and this metabolite is reversible in humans to a limited extent (< 5%). These metabolites are inactive as COX-1 or COX-2 inhibitors. Cytochrome P450 plays a minor role in metabolism of rofecoxib.
The metabolism of rofecoxib, a potent and selective inhibitor of cyclooxygenase-2, was examined in vitro using human liver subcellular fractions. The biotransformation of rofecoxib was highly dependent on the subcellular fraction and the redox system used. In liver microsomal incubations, NADPH-dependent oxidation of rofecoxib to 5-hydroxyrofecoxib predominated, whereas NADPH-dependent reduction of rofecoxib to the 3,4-dihydrohydroxy acid metabolites predominated in cytosolic incubations. In incubations with S9 fractions, metabolites resulting from both oxidative and reductive pathways were observed. In contrast to microsomes, the oxidation of rofecoxib to 5-hydroxyrofecoxib by S9 fractions followed two pathways, one NADPH-dependent and one NAD+-dependent (non-cytochrome P450), with the latter accounting for about 40% of total activity. The 5-hydroxyrofecoxib thus formed was found to undergo NADPH-dependent reduction ("back reduction") to rofecoxib in incubations with liver cytosolic fractions. In incubations with dialyzed liver cytosol, net hydration of rofecoxib to form 3,4-dihydro-5-hydroxyrofecoxib was observed, whereas the 3,4-dihydrohydroxy acid derivatives were formed when NADPH was present. Although 3,4-dihydro-5-hydroxyrofecoxib could be reduced to the 3,4-dihydrohydroxy acid by cytosol in the presence of NADPH, the former species does not appear to serve as an intermediate in the overall reductive pathway of rofecoxib metabolism. In incubations of greater than 2 h with S9 fractions, net reductive metabolism predominated over oxidative metabolism. These in vitro results are consistent with previous findings on the metabolism of rofecoxib in vivo in human and provide a valuable insight into mechanistic aspects of the complex metabolism of this drug.
Metabolism of rofecoxib is primarily mediated through reduction by cytosolic enzymes. The principal metabolic products are the cis-dihydro and trans-dihydro derivatives of rofecoxib, which account for nearly 56% of recovered radioactivity in the urine. An additional 8.8% of the dose was recovered as the glucuronide of the hydroxy derivative, a product of oxidative metabolism. The biotransformation of rofecoxib and this metabolite is reversible in humans to a limited extent (<5%). Theses metabolites are inactive as COX-1 or COX-2 inhibitors.
Rofecoxib has known human metabolites that include 5-hydroxy-rofecoxib.
Biological Half-Life
17 hours
Approximately 17 hours.
Toxicity/Toxicokinetics
Hepatotoxicity
In clinical studies involving several thousand patients treated for at least 3 months, the rate of serum aminotransferase enzyme elevations above three times the upper limit of the normal range was 1.8% in rofecoxib treated compared to 0.3% in placebo treated patients and 0.1-0.4% in patients receiving other common NSAIDs. Thus, ALT elevations due to rofecoxib were uncommon and usually of minimal clinical significance, resolving even with drug continuation.
In rare instances, rofecoxib can cause clinically apparent, symptomatic drug induced liver injury with jaundice. The pattern of liver enzyme elevations has usually been cholestatic or mixed (Case 1), although hepatocellular patterns of injury have also been described. The latency to onset of liver injury was extremely variable, ranging from a few weeks to several years, but was typically within 1 to 12 weeks of starting. Autoimmune and immunoallergic features were uncommon.
Likelihood score: C (probable rare cause of clinically apparent liver injury).
Protein Binding
87%
Interactions
Concurrent use /of rifampin/ with rofecoxib may decrease rofecoxib plasma concentrations by 50%; ... .
Rofecoxib 75 mg per day for 10 days increased plasma methotrexate concentrations by 23% in patients receiving methotrexate 7.5 to 15 mg/week; the effect of recommended doses of rofecoxib in unknown; therefore, monitoring for methotrexate toxicity is recommended.
Concurrent use /of aspirin/ with rofecoxib may increase the risk for gastrointestinal (GI) ulcerations or GI complications.
The administration of rofecoxib with calcium carbonate-, aluminum- or magnesium-containing antacids decreased the area under the plasma concentration-time curve (AUC) by 13% and 8%, respectively, in elderly patients; the peak plasma concentration of rofecoxib was decreased by approximately 20% for both antacids.
For more Interactions (Complete) data for ROFECOXIB (14 total), please visit the HSDB record page.
References

[1]. Rofecoxib [Vioxx, MK-0966; 4-(4'-methylsulfonylphenyl)-3-phenyl-2-(5H)-furanone]: a potent and orally active cyclooxygenase-2 inhibitor. Pharmacological and biochemical profiles. J Pharmacol Exp Ther. 1999 Aug;290(2):551-60.

[2]. Rofecoxib inhibits retinal neovascularization via down regulation of cyclooxygenase-2 and vascular endothelial growth factor expression. Clin Exp Ophthalmol. 2015 Jul;43(5):458-65.

[3]. Synergistic effect of gefitinib and rofecoxib in mesothelioma cells. Mol Cancer. 2010 Feb 2;9:27.

Additional Infomation
Rofecoxib is a butenolide that is furan-2(5H)-one substituted by a phenyl group at position 3 and by a p-(methylsulfonyl)phenyl group at position 4. A selective cyclooxygenase 2 inhibitor, it was used from 1999 to 2004 for the treatment of ostoarthritis, but was withdrawn following concerns about an associated increased risk of heart attack and stroke. It has a role as a cyclooxygenase 2 inhibitor, a non-steroidal anti-inflammatory drug and an analgesic. It is a sulfone and a butenolide.
Rofecoxib is used for the treatment of osteoarthritis, rheumatoid arthritis, acute pain in adults, and primary dysmenorrhea, as well as acute treatment of migraine attacks with or without auras. Rofecoxib is a solid. This compound belongs to the stilbenes. These are organic compounds containing a 1,2-diphenylethylene moiety. Stilbenes (C6-C2-C6 ) are derived from the common phenylpropene (C6-C3) skeleton building block. The introduction of one or more hydroxyl groups to a phenyl ring lead to stilbenoids. Rofecoxib has a half-life of 17 hours and its mean oral bioavailability at therapeutically recommended doses of 125, 25, and 50 mg is approximately 93%. The proteins that rofecoxib target include elastin and prostaglandin G/H synthase 2. Cytochrome P450 1A2, Cytochrome P450 3A4, Cytochrome P450 2C9, Cytochrome P450 2C8, and Prostaglandin G/H synthase 1 are known to metabolize rofecoxib. On September 30, 2004, Merck voluntarily withdrew rofecoxib from the market because of concerns about increased risk of heart attack and stroke associated with long-term, high-dosage use.
Rofecoxib is a nonsteroidal antiinflammatory drug (NSAID) that selectively inhibits cyclooxgenase-2 (Cox-2), which was used in the therapy of chronic arthritis and mild-to-moderate musculoskeletal pain. Rofecoxib was withdrawn in 2004 because of an association with an increase in cardiovascular events with its long term use. Rofecoxib had also been linked transient serum aminotransferase elevations during therapy and to rare instances of idiosyncratic drug induced liver disease.
Rofecoxib is a synthetic, nonsteroidal derivative of phenyl-furanone with antiinflammatory, antipyretic and analgesic properties and potential antineoplastic properties. Rofecoxib binds to and inhibits the enzyme cyclooxygenase-2 (COX-2), resulting in an inhibition of the conversion of arachidonic acid to prostaglandins. COX-related metabolic pathways may represent key regulators of cell proliferation and neo-angiogenesis. Some epithelial tumor cell types overexpress pro-angiogenic COX-2. (NCI04)
Drug Indication
For the treatment of osteoarthritis, rheumatoid arthritis, acute pain in adults, and primary dysmenorrhea, as well as acute treatment of migraine attacks with or without auras.
FDA Label
Mechanism of Action
The anti-inflammatory, analgesic, and antipyretic effects of NSAIDs appear to result from the inhibition of prostaglandin synthesis. Although the exact mechanism of action has not been determined, these effects appear to be mediated through the inhibition of the COX-2 isoenzyme at the sites of inflammation with subsequent reduction in the synthesis of certain prostaglandins from their arachidonic acid precursors. Rofecoxib selectively inhibits the cyclooxygenase-2 (COX-2) enzyme, which is important for the mediation of inflammation and pain. Unlike non-selective NSAIDs, rofecoxib does not inhibit platelet aggregation. It also has little to no affinity for COX-1.
Rofecoxib is a nonsteroidal anti-inflammatory drug (NSAID) with anti-inflammatory, analgesic, and antipyretic therapeutic effects. It has been proposed that rofecoxib inhibits the activity of the enzyme cyclooxygenase-2 (COX-2), resulting in a decreased formation of precursors of prostaglandins. Rofecoxib does not inhibit cyclooxygenase-1 (COX-1) isoenzyme in humans at therapeutic concentrations.
Therapeutic Uses
/September 20, 2004/ Merck & Co., Inc. announced a voluntary withdrawal of Vioxx (rofecoxib) from the U.S. and worldwide market due to safety concerns of an increased risk of cardiovascular events (including heart attack and stroke) in patients on Vioxx. Vioxx is a prescription COX-2 selective, non-steroidal anti-inflammatory drug (NSAID) that was approved by FDA in May 1999 for the relief of the signs and symptoms of osteoarthritis, for the management of acute pain in adults, and for the treatment of menstrual symptoms, and was later approved for the relief of the signs and symptoms of rheumatoid arthritis in adults and children.
Anti-inflammatory.
Rofecoxib is indicated for the relief of the signs and symptoms of osteoarthritis. /Included in US product labeling/
Rofecoxib is indicated for short-term use (5 days) for relief of acute pain, especially when anti-inflammatory actions may be desired, such as following dental or orthopedic surgery. /Included in US product labeling/
Rofecoxib is indicated for short-term use (5 days) for relief of the pain and other symptoms of primary dysmenorrhea. /Included in US product labeling
Drug Warnings
/Merck & Co., Inc. announced a voluntary withdrawal of Vioxx (rofecoxib) from the U.S. and worldwide market/ due to safety concerns of an increased risk of cardiovascular events (including heart attack and stroke) in patients on Vioxx. Vioxx is a prescription COX-2 selective, non-steroidal anti-inflammatory drug (NSAID) that was approved by FDA in May 1999 for the relief of the signs and symptoms of osteoarthritis, for the management of acute pain in adults, and for the treatment of menstrual symptoms, and was later approved for the relief of the signs and symptoms of rheumatoid arthritis in adults and children.
There is controversy whether cyclooxygenase-2 (COX-2) specific inhibitors are associated with elevations in blood pressure requiring treatment in typical clinical practice. We examined the risk of new onset hypertension in a retrospective case-control study involving 17 844 subjects aged > or =65 years from 2 US states. Multivariable logistic models were examined to assess the relative risk of new onset hypertension requiring treatment in patients who used celecoxib or rofecoxib compared with patients taking either the other COX-2 specific inhibitor, a nonspecific NSAID, or no NSAID. During the 1999 to 2000 study period, 3915 patients were diagnosed and began treatment for hypertension; 4 controls were selected for every case. In no model was celecoxib significantly associated with the development of hypertension. Rofecoxib users were at a significantly increased relative risk of new onset hypertension compared with patients taking celecoxib (odds ratio (OR) 1.6; 95% confidence interval (CI), 1.2 to 2.1), taking a nonspecific NSAID (OR 1.4; 95% CI, 1.1 to 1.9), or taking no NSAID (OR 1.6; 95% CI, 1.3 to 2.0). There were no clear dosage or duration effects. In patients with a history of chronic renal disease, liver disease, or congestive heart failure, the relative risk of new onset hypertension was twice as high in those taking rofecoxib compared with celecoxib (OR 2.1; 95% CI, 1.0 to 4.3). In this retrospective case-control study of patients aged > or =65 years, rofecoxib use was associated with an increased relative risk of new onset hypertension; this was not seen in patients taking celecoxib.
In a double-blind study, 35 stable subjects on low-dose aspirin with > or = 2 previous acute coronary events and 2 of 2 screening CRP values >2.0 mg/L were randomized to the COX-2 inhibitor rofecoxib (25 mg) or placebo daily for 6 months. Serum CRP, interleukin-6 (IL-6), P-selectin, matrix metalloproteinase-9 (MMP-9), and brachial artery endothelial function were evaluated. In the placebo group, CRP (median) was 3.16 mg/L (25% and 75% quartiles, 1.90 and 5.78 mg/L) at baseline and 4.22 mg/L (25% and 75% quartiles, 2.04 and 6.25 mg/L) at 6 months; in the rofecoxib group, CRP was 3.45 mg/L (25% and 75% quartiles, 2.08 and 5.78 mg/L) at baseline and 1.41 mg/L (25% and 75% quartiles, 1.17 and 4.81 mg/L) at 6 months (P=0.03). Rofecoxib compared with placebo also lowered IL-6 at 6 months (P=0.0002). There was a significant off-drug effect on CRP and IL-6 levels in the rofecoxib group 3 months after treatment (P=0.005 and P=0.009, respectively). Rofecoxib did not significantly affect P-selectin, MMP-9, and brachial artery vasoreactivity. Prolonged COX-2 inhibition attenuates CRP and IL-6, does not modify P-selectin and MMP-9, and has no deleterious effect on endothelial function in stable patients with a history of recurrent acute coronary events and raised CRP. These results strengthen the rationale for evaluating the clinical benefit of COX-2 inhibition in patients with ischemic heart disease.
A 73-year-old woman was prescribed rofecoxib 25 mg/day for rheumatoid arthritis in addition to other medications on which the patient had been stabilized. Six months after initiation of rofecoxib, linear plaques over the infra-orbital and bitemporal areas of both eyes were observed. Several itchy violaceous papules also developed on her right wrist and dorsum of the left foot. She also had a hyperpigmented macule on her right buccal mucosa. As the skin rash was localized and the patient was initially unwilling to undergo skin biopsy, rofecoxib was continued and a topical steroid was started. One month later, the patient was seen in the dermatology clinic, and the improvement of her skin reaction was significant. A skin biopsy performed during this visit was consistent with LDE. On the next day, her rheumatologist decided to discontinue the offending drug, rofecoxib. Two months later, all skin lesions had completely resolved. No rechallenge with rofecoxib was attempted. LDE is a rare skin reaction that can be associated with several drugs. Rofecoxib, a cyclooxygenase-2 inhibitor, has never before been reported to cause LDE. An objective causality assessment indicates that rofecoxib was the probable cause of the skin reaction.
For more Drug Warnings (Complete) data for ROFECOXIB (31 total), please visit the HSDB record page.
Pharmacodynamics
Rofecoxib, a selective cyclooxygenase-2 (COX-2) inhibitor, is classified as a nonsteroidal anti-inflammatory drug (NSAID). Unlike celecoxib, rofecoxib lacks a sulfonamide chain and does not require CYP450 enzymes for metabolism. Like other NSAIDs, rofecoxib exhibits anti-inflammatory, analgesic, and antipyretic activity. NSAIDs appear to inhibit prostaglandin synthesis via the inhibition of cyclooxygenase (COX), which are responsible for catalyzing the formation of prostaglandins in the arachidonic acid pathyway. There are at least two isoenzymes, COX-1 and COX-2, that have been identified. Although the exact mechanisms have not been clearly established, NSAIDs exert their anti-inflammatory, analgesic, and antipyretic primarily through the inhibition of COX-2. The inhibition of COX-1 is principally responsible for the negative effects on the GI mucosa. As rofecoxib is selective for COX-2, it may be potentially associated with a decreased risk of certain adverse events, but more data is needed to fully evaulate the drug.
These protocols are for reference only. InvivoChem does not independently validate these methods.
Physicochemical Properties
Molecular Formula
C17H14O4S
Molecular Weight
314.36
Exact Mass
314.061
CAS #
162011-90-7
Related CAS #
Rofecoxib-d5;544684-93-7
PubChem CID
5090
Appearance
Light yellow to green solid powder
Density
1.3±0.1 g/cm3
Boiling Point
577.6±50.0 °C at 760 mmHg
Melting Point
207°C
Flash Point
303.1±30.1 °C
Vapour Pressure
0.0±1.6 mmHg at 25°C
Index of Refraction
1.619
LogP
1.34
Hydrogen Bond Donor Count
0
Hydrogen Bond Acceptor Count
4
Rotatable Bond Count
3
Heavy Atom Count
22
Complexity
556
Defined Atom Stereocenter Count
0
InChi Key
RZJQGNCSTQAWON-UHFFFAOYSA-N
InChi Code
InChI=1S/C17H14O4S/c1-22(19,20)14-9-7-12(8-10-14)15-11-21-17(18)16(15)13-5-3-2-4-6-13/h2-10H,11H2,1H3
Chemical Name
3-(4-methylsulfonylphenyl)-4-phenyl-2H-furan-5-one
Synonyms
MK-0966; MK0966; MK0966; MK966; MK966; MK 966; MK 0966; Trade name: Vioxx; Ceoxx; Ceeoxx.
HS Tariff Code
2934.99.9001
Storage

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

Shipping Condition
Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)
Solubility Data
Solubility (In Vitro)
DMSO: 63 mg/mL (200.4 mM)
Water:<1 mg/mL
Ethanol:<1 mg/mL
Solubility (In Vivo)
Solubility in Formulation 1: ≥ 2.5 mg/mL (7.95 mM) (saturation unknown) in 10% DMSO + 90% Corn Oil (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 25.0 mg/mL clear DMSO stock solution to 900 μL of corn oil and mix evenly.

Solubility in Formulation 2: 30% PEG400+0.5% Tween80+5% propylene glycol: 30mg/mL

 (Please use freshly prepared in vivo formulations for optimal results.)
Preparing Stock Solutions 1 mg 5 mg 10 mg
1 mM 3.1811 mL 15.9053 mL 31.8107 mL
5 mM 0.6362 mL 3.1811 mL 6.3621 mL
10 mM 0.3181 mL 1.5905 mL 3.1811 mL

*Note: Please select an appropriate solvent for the preparation of stock solution based on your experiment needs. For most products, DMSO can be used for preparing stock solutions (e.g. 5 mM, 10 mM, or 20 mM concentration); some products with high aqueous solubility may be dissolved in water directly. Solubility information is available at the above Solubility Data section. Once the stock solution is prepared, aliquot it to routine usage volumes and store at -20°C or -80°C. Avoid repeated freeze and thaw cycles.

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Clinical Trial Information
NCT Number Recruitment interventions Conditions Sponsor/Collaborators Start Date Phases
NCT04684511 Terminated Drug: TRM-201 (Rofecoxib)
Drug: Placebo
Hemophilic Arthropathy Tremeau Pharmceuticals, Inc. June 2, 2021 Phase 3
NCT00038389 Terminated Drug: Vioxx Glioma
Brain Neoplasms
M.D. Anderson Cancer Center October 2001 Phase 1
NCT00568295 Completed Drug: acetaminophen
Drug: Rofecoxib
Osteoarthritis of the Knee Johnson & Johnson Consumer and
Personal Products Worldwide
October 1999 Phase 3
NCT00060476 Completed Drug: rofecoxib
Drug: Comparator: placebo (unspecified)
Prostate Cancer Merck Sharp & Dohme LLC January 8, 2003 Phase 3
Biological Data
  • Rofecoxib

    Inhibitory effect of rofecoxib or indomethacin in rodent models of inflammation, pain, and pyresis.J Pharmacol Exp Ther.1999 Aug;290(2):551-60.
  • Rofecoxib

    Inhibition of arachidonic acid-induced PGE2 formation in LPS-stimulated dog whole blood ex vivo by rofecoxib or diclofenac.J Pharmacol Exp Ther.1999 Aug;290(2):551-60.
  • Rofecoxib

    Effects of acute or chronic (5 days b.i.d.) dosing of rofecoxib, diclofenac, or indomethacin on gastrointestinal integrity in rats.J Pharmacol Exp Ther.1999 Aug;290(2):551-60.
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