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Celebrex (Celecoxib)

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Generic Celebrex is a high-powered medication in battle against arthritis (rheumatoid arthritis, osteoarthritis), ankylosing spondylitis and painful menstruation. Generic Celebrex can be helpful for patients with problems of stomach, intestines, heart, circulation, and FAP (familial adenomatous polyposis). Generic Celebrex acts as popular medicine which can not only provide treatment of arthritis but also it protects from painful menstruation.

Other names for this medication:

Similar Products:
Motrin, Naprosyn, Anaprox, Mobic, Indocin


Also known as:  Celecoxib.


Generic Celebrex is produced with efficacious pharmacy formula making Generic Celebrex wonderful weapon against arthritis (rheumatoid arthritis, osteoarthritis), painful menstruation, inflammation, fever, joint pain, swelling and tenderness. Target of Generic Celebrex is to prevent pain and inflammation.

Generic Celebrex acts as popular medicine which can not only provide treatment of arthritis but also it protects from painful menstruation. Generic Celebrex acts blocking hormones of pain and inflammation.

Celebrex is also known as Celecoxib, Celebra, Cobix, Celcoxx, Selecap.

Generic Celebrex is NSAID (anti-inflammatory drug).

Generic name of Generic Celebrex is Celecoxib.

Brand names of Generic Celebrex are Celebrex, Celebra.


Generic Celebrex is available in capsules which should be taken by mouth meal or milk.

It is better to take Generic Celebrex every day.

Take Generic Celebrex and remember that its dosage depends on patient's health state.

For treatment of rheumatoid arthritis

Usual Generic Celebrex dosage is 100-200 mg twice a day.

For treatment of osteoarthritis

Usual Generic Celebrex dosage is 100 mg twice a day or 200 mg once a day.

For treatment of painful menstruation

Usual Generic Celebrex dosage is 400 mg once a day at the first day of treatment. In case you need, the dosage of 400 mg can be divided into double dose and can be taken twice a day.

For treatment of FAP

Usual Generic Celebrex dosage 400 mg twice a day.

If you want to achieve most effective results do not stop taking Generic Celebrex suddenly.


If you overdose Generic Celebrex and you don't feel good you should visit your doctor or health care provider immediately.


Store at room temperature between 15 and 30 degrees C (59 and 86 degrees F) away from moisture and heat. Keep container tightly closed. Throw away any unused medicine after the expiration date. Keep out of the reach of children.

Side effects

The most common side effects associated with Celebrex are:

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Side effect occurrence does not only depend on medication you are taking, but also on your overall health and other factors.


Do not take Generic Celebrex if you are allergic to Generic Celebrex components or to aspirin.

Do not take Generic Celebrex if you are pregnant, planning to become pregnant. It is unknown if Generic Celebrex is excreted in breast milk. Avoid breast-feeding.

Generic Celebrex can't be given to children under 2 years.

Generic Celebrex can't be given to patients who experience bypass surgery.

Do not use allergy and pain medicines at the same time with Generic Celebrex.

Try to be careful with Generic Celebrex in case of using such medications as (Mavik), quinapril (Accupril), ACE inhibitor (captopril (Capoten), benazepril (Lotensin), lisinopril (Zestril, Prinivil), ramipril (Altace), enalapril (Vasotec), fosinopril (Monopril), moexipril (Univasc), perindopril (Aceon), blood thinner as warfarin (Coumadin), aspirin or other NSAIDs (mefenamic acid (Ponstel), etodolac (Lodine), diclofenac (Voltaren), ibuprofen (Advil, Motrin), piroxicam (Feldene),naproxen (Aleve, Naprosyn), flurbiprofen (Ansaid), ketorolac (Toradol), ketoprofen (Orudis), nabumetone (Relafen), meloxicam (Mobic)), methotrexate (Rheumatrex, Trexall), diuretics (furosemide (Lasix)), lithium (Eskalith, Lithobid).

Be careful with Generic Celebrex in case of having liver, heart or kidney disease, asthma, high blood pressure, stroke, stomach ulcers, bleeding or blood clotting disorder, congestive heart failure, epilepsy.

Be careful with sunbeams. Generic Celebrex makes skin sensitive to sunlight. Protect skin from the sun.

Avoid alcohol.

It can be dangerous to stop Generic Celebrex taking suddenly.

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Design, synthesis and pharmacological activities of a group of 1,3,5-trisubstituted pyrazolines were reported. The chemical structures of the synthesized compounds have been assigned on the basis of IR, MS, (1)H NMR, and (13)C NMR spectral analyses. The synthesized 1,3,5-trisubstituted pyrazoline derivatives were evaluated in vivo for anti-inflammatory, analgesic activities and in vitro for COX-1/2 inhibition assay. Among the tested compounds, derivatives 4h, 6e, 7a, 7e, and 9 showed more potent anti-inflammatory and analgesic activities than the reference drug celecoxib. On the basis of their higher activities in the in vivo studies compared with celecoxib, the five compounds 4h, 6e, 7a, 7e and 9 were selected to test their inhibitory activities against ovine COX-1/2 using an in vitro cyclooxygenase inhibition assay. Docking study of compounds 7a, 7e and 9 into the COX-2 binding site revealed a similar binding mode to SC-558, a selective COX-2 inhibitor.

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Lewis lung carcinoma cells (LLCCs) were injected into the intramedullary space of the femur of wild-type (WT) and PGES-1-/- mice. Pain-related behaviors were evaluated.

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Treatment with the COX-2 inhibitors celecoxib and CAY10404 or knockdown of COX-2 significantly inhibited prostate cancer cell proliferation. Flow-cytometric analysis and immunofluorescent staining confirmed the cell cycle arrested at the G2/M phase. Biochemical analysis showed that inhibition of COX-2 or suppression of COX-2 expression induced a dramatic down-regulation of key proteins in the kinetochore/centromere assembly, such as ZWINT, Cdc20, Ndc80, CENP-A, Bub1, and Plk1. Furthermore, the EP1 receptor antagonist SC51322, but not the EP2, EP3, and EP4 receptor antagonists, produced similar effects to the COX-2 inhibitors on cell proliferation and down-regulation of kinetochore/centromere proteins, suggesting that the effect of the COX-2 inhibition is through inactivation of the EP1 receptor signaling.

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To review extant literature implicating inflammation in the pathophysiology of bipolar disorder. Furthermore, we review evidence regarding the anti-inflammatory actions of mood-stabilizing medication, the putative reciprocal association of inflammation with behavioral parameters and medical burden in bipolar disorder, and the potential role of anti-inflammatory agents in the treatment of bipolar disorder.

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ATB-346 suppressed gastric prostaglandin E(2) synthesis as effectively as naproxen, but produced negligible damage in the stomach and intestine. In situations in which the gastric mucosa was rendered significantly more susceptible to naproxen-induced damage (e.g. ablation of sensory afferent nerves, inhibition of endogenous nitric oxide or hydrogen sulphide synthesis, co-administration with aspirin, antagonism of K(IR)6.x channels), ATB-346 did not cause significant damage. Unlike naproxen and celecoxib, ATB-346 accelerated healing of pre-existing gastric ulcers. In a mouse airpouch model, ATB-346 suppressed cyclooxygenase-2 activity and inhibited leukocyte infiltration more effectively than naproxen. ATB-346 was as effective as naproxen in adjuvant-induced arthritis in rats, with a more rapid onset of activity. Unlike naproxen, ATB-346 did not elevate blood pressure in hypertensive rats.

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Complexation of caffeine with the drug celecoxib was used to enhance its solubility as well as in vitro dissolution in the present investigation. Caffeine was extracted from tea leaves using the sublimation method. A molecular complex (1:1) of caffeine-celecoxib was prepared using the solubility method. The solubility of celecoxib in distilled water and the caffeine complex was determined using a HPLC method at a wavelength of 250 nm. Dissolution studies of pure celecoxib, a marketed capsule (Celebrex), and the complex were performed using USP dissolution apparatus I for pure celecoxib and the complex and apparatus II for the capsule in distilled water. The highest solubility (48.32 mg/mL) as well as percent dissolution (90.54%) of celecoxib was obtained with the caffeine-celecoxib complex. The results for solubility and dissolution were highly significant as compared to pure celecoxib and the marketed capsule (p < 0.01). These results suggest that caffeine is a promising complexing agent for solubility as well as dissolution enhancement of the poorly soluble drug celecoxib.

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A previous study has shown celecoxib 100 mg b.i.d. to be comparably effective to naproxen 500 mg b.i.d. in treating osteoarthritis (OA). The primary objective of this study was to compare the efficacy of a once-daily regimen of celecoxib (200 mg q.d.) to the 100 mg b.i.d. regimen in treating the signs and symptoms of OA. In this double-blind, placebo-controlled, parallel-group, multicenter study, 686 patients with OA of the knee in a flare state were enrolled. Patients were randomly assigned to receive celecoxib 100 mg b.i.d. (N = 231), celecoxib 200 mg q.d. (N = 223), or the placebo (N = 232) for 6 weeks. Arthritis assessments were performed at baseline and at weeks 2 and 6, or at early termination. In all measurements of efficacy, at all assessments, improvements from baseline in both celecoxib groups were statistically superior to those in the placebo group (p

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Three co-primary efficacy endpoints were mean change from baseline to week 12 in Western Ontario and McMaster Osteoarthritis Index (WOMAC) pain and function subscales, and Patient Global Assessment of osteoarthritis using a visual analog scale (PGA-VAS).

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Pancreatic cancer is a lethal disease that is resistant to chemotherapy and radiotherapy. Gemcitabine has recently been shown to be an improvement over 5-fluorouracil in patients with advanced disease. It is also a potent radiosensitizer, which has led to the investigation of gemcitabine with concurrent radiotherapy. However, preliminary results indicate that there are significant limitations to this approach in this challenging disease. Pancreatic cancer cells have alterations in many molecular signaling pathways that may be responsible for their resistance to cytotoxic therapy and aggressive behavior. Cyclooxygenase-2 (COX-2) is commonly overexpressed in pancreatic tumors, and preclinical evidence indicates that selective COX-2 inhibition enhances both chemotherapy and radiotherapy response, without affecting normal tissue damage. We have initiated preclinical studies as well as a phase I clinical protocol evaluating the combination of gemcitabine and celecoxib (Celebrex) with radiotherapy. In preclinical studies, celecelecoxib strongly enhanced the antitumor efficacy of chemoradiation. However, preliminary observations from both the preclinical experiments as well as the clinical protocol have revealed more toxicity with this combination than with gemcitabine and radiotherapy alone. These observations require further study, but are cause for concern when combining gemcitabine, radiotherapy, and celecoxib.

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Randomized double blind placebo controlled trial.

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Neoadjuvant use of FEC-T with concurrent CXB is active and safe for treatment of operable invasive breast cancer. The ORR was higher, but QpCR was comparable to other studies. Most patients are still disease-free, and BCT became an option for the females. Further clinical and translational studies on the use of cyclooxygenase-2 inhibitors with neoadjuvant chemotherapy are warranted.

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In several neoplastic diseases, including hepatocellular carcinoma, the expression of P-glycoprotein and cyclooxygenase-2 (COX-2) are often increased and involved in drug resistance and poor prognosis. P-glycoprotein, in addition to drug resistance, blocks cytochrome c release, preventing apoptosis in tumor cells. Because COX-2 induces P-glycoprotein expression, we evaluated the effect of celecoxib, a specific inhibitor of COX-2 activity, on P-glycoprotein-mediated resistance to apoptosis in cell lines expressing multidrug resistant (MDR) phenotype. Experiments were done using MDR-positive and parental cell lines at basal conditions and after exposure to 10 or 50 micromol/L celecoxib. We found that 10 micromol/L celecoxib reduced P-glycoprotein, Bcl-x(L), and Bcl-2 expression, and induced translocation of Bax from cytosol to mitochondria and cytochrome c release into cytosol in MDR-positive hepatocellular carcinoma cells. This causes the activation of caspase-3 and increases the number of cells going into apoptosis. No effect was shown on parental drug-sensitive or on MDR-positive hepatocellular carcinoma cells after transfection with MDR1 small interfering RNA. Interestingly, although inhibiting COX-2 activity, 50 micromol/L celecoxib weakly increased the expression of COX-2 and P-glycoprotein and did not alter Bcl-x(L) and Bcl-2 expression. In conclusion, these results show that relatively low concentrations of celecoxib induce cell apoptosis in MDR cell lines. This effect is mediated by P-glycoprotein and suggests that the efficacy of celecoxib in the treatment of different types of cancer may depend on celecoxib concentration and P-glycoprotein expression.

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Rheumatoid arthritis (RA) is a systemic inflammatory disease that mainly affects the articular synovial tissues. Although the etiology of RA has not yet been elucidated, physical and biochemical inhibition of synovial hyperplasia, which is the origin of articular destruction, may be an effective treatment for RA. Nonsteroidal anti-inflammatory drugs (NSAIDs) have long been used for the treatment of RA. The mechanism of action of NSAIDs generally involves the inhibition of cyclooxygenase (COX) at sites of inflammation. Thus, NSAIDs were not generally considered to have a so-called anti-rheumatic effect, including inhibition of progressive joint destruction and induction of remission. However, certain conventional NSAIDs and celecoxib, a selective COX-2 inhibitor, have been reported to inhibit synovial hyperplasia by inducing the apoptosis of human synovial fibroblasts. Therefore, it has been suggested that such NSAIDs may not only have an anti-inflammatory effect but also an anti-rheumatic effect. In this review, we summarize findings about the pro-apoptotic effect, in other words, anti-proliferative effect of NSAIDs on synovial fibroblasts from patients with RA.

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Many studies have shown that a variety of strategies, including the use of cyclooxygenase-2 (COX-2) inhibitors, or co-prescription of misoprostol or proton pump inhibitors, result in reduced endoscopic damage and ulceration compared with non-selective nonsteroidal anti-inflammatory drugs (NSAIDs) alone. Questions have been raised as to whether this would translate into improved clinical outcomes. Consequently, several studies have investigated whether use of COX-2 inhibitors (Vioxx Gastrointestinal Outcomes Research [VIGOR] and the Celecoxib Long-Term Arthritis Safety Assessment Study [CLASS] studies) or co-prescription with misoprostol (MUCOSA) would reduce the event rate of clinically significant ulcers. These studies have shown an approximate halving of such events. They have raised the possibility that use of low dose aspirin may compromise these benefits and appear to have shown differences between (at least some) COX-2 inhibitors and (at least some) NSAIDs with regard to myocardial infarction. Among the lessons learned from this experience are the need to define closely the outcomes of interest and possibly to concentrate on ulcer complications, the need for adequately powered studies, and the fact that endoscopic studies broadly predict outcomes. However, there are differences in the estimated rates of reduction. It is not self evident whether outcomes studies or endoscopic studies give a truer estimate of risk. A helpful development would be more standardized gastrointestinal assessment at the time of ulcer complications and this could be achieved if studies were done in countries with well-developed primary care systems.

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Abdominoplasty, the treatment for abdominal wall deformity stemming from weight loss after bariatric surgery, can cause postoperative anemia. Moreover, bariatric surgery has been associated with iron deficiency, which by itself can compromise erythropoiesis. The objective of this research is to describe the development of anemia after postbariatric abdominoplasty.

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The median size of the dominant liver metastasis was 10 cm (range, 3-19 cm). Twelve patients (71%) had evidence of extrahepatic disease. A median of 2 (range, 0-4) prior chemotherapy regimens had been administered. Median radiation dose was 42 Gy (range, 7.5-72 Gy). Concurrent chemotherapy included celecoxib in 1 (6%), capecitabine in 6 (35%), and both agents in 9 (53%) patients. Frequencies of acute diarrhea, nausea, vomiting, fatigue, hand-foot syndrome, and neutropenia were 29%, 47%, 6%, 29%, 7%, and 0%, respectively (all grade 2 or lower; no grade 3 toxicities). No late toxicities were noted. With a median follow-up time of 9.2 months, the median actuarial overall survival time from RT was 12.6 months (95% confidence interval [CI]: 3.3-40.9 months). The actuarial in-field local control rate was 62% at 6 months. The median actuarial time to in-field, out-of-field hepatic and distant progression were 6.8, 3.9, and 4.1 month, respectively (95% CIs, 3.9-15.8, 1.8-6.3, and 1.8-11.5 months, respectively).

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COX-2 and prostaglandins (PGs) might play important roles in epilepsy. In kainic acid-induced seizures, the brain largely increases PGD(2), first from COX-1 and later COX-2-induced PGF(2alpha). Pre-treatment with COX-2 inhibitors such as indomethacin, nimesulide, and celecoxib is known to aggravate kainic acid (KA)-induced seizure activity. However it is not known whether the proconvulsant effect of those non-steroidal anti-inflammatory drugs (NSAIDs) is due to changes in endogenous prostaglandins (PGs), or what types of PGs are involved. The purpose of this study was to determine the effect of intracisternally administered PGs on KA-induced seizures aggravated by pre- or post-treatment with COX-2 inhibitors. Systemic KA injection (10 mg/kg i.p.) in mice evoked mild seizure activity within 15 min. PGs were administrated intracisternally 20 min prior to KA administration. COX inhibitors (indomethacin, nimesulide, and ketoprofen, 10 mg/kg i.p.) were injected 1 h before or 15 min after KA. An additional COX-2 inhibitor, celecoxib, was administered orally. Intracisternally administered PGF(2alpha) (700 ng), but not PGD(2) (700 ng) or PGE(2) (700 ng) completely alleviated KA-induced seizures potentiated by COX-2 inhibitors, and also reduced KA-induced hippocampal neuronal death aggravated by indomethacin. PGF(2alpha) alone did not affect KA-induced seizures. However, an FP receptor antagonist, AL 8810 (10 or 50 ng) which is an 11beta-fluoro analogue of PGF(2alpha) potentiated KA-induced seizure activity dose-dependently. In summary, pre- or post-treatment with COX-2 inhibitors aggravates KA-induced seizures, which suggests to change the endogenous PGF(2alpha). Seizure-induced PGF(2alpha) might act as an endogenous anticonvulsant through FP receptors.

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Numerous experimental, epidemiologic, and clinical studies suggest that nonsteroidal anti-inflammatory drugs (NSAIDs), particularly the highly selective cyclooxygenase (COX)-2 inhibitors, have promise as anticancer agents. NSAIDs restore normal apoptosis in human adenomatous colorectal polyps and in various cancer cell lines that have lost adenomatous polyposis coli gene function. NSAIDs also inhibit angiogenesis in cell culture and rodent models of angiogenesis. Many epidemiologic studies have found that long-term use of NSAIDs is associated with a lower risk of colorectal cancer, adenomatous polyps, and, to some extent, other cancers. Two NSAIDs, sulindac and celecoxib, have been found to inhibit the growth of adenomatous polyps and cause regression of existing polyps in randomized trials of patients with familial adenomatous polyposis (FAP). However, unresolved questions about the safety, efficacy, optimal treatment regimen, and mechanism of action of NSAIDs currently limit their clinical application to the prevention of polyposis in FAP patients. Moreover, the development of safe and effective drugs for chemoprevention is complicated by the potential of even rare, serious toxicity to offset the benefit of treatment, particularly when the drug is administered to healthy people who have low annual risk of developing the disease for which treatment is intended. This review considers generic approaches to improve the balance between benefits and risks associated with the use of NSAIDs in chemoprevention. We critically examine the published experimental, clinical, and epidemiologic literature on NSAIDs and cancer, especially that regarding colorectal cancer, and identify strategies to overcome the various logistic and scientific barriers that impede clinical trials of NSAIDs for cancer prevention. Finally, we suggest research opportunities that may help to accelerate the future clinical application of NSAIDs for cancer prevention or treatment.

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NSAIDs work by inhibiting the enzyme cyclo-oxygenase (COX), responsible for prostaglandin synthesis. This enzyme exists in two isoforms, COX-1 and COX-2. Inhibition of COX-1 is thought to be the main cause of the gastrointestinal unwanted effects of NSAIDs, whilst inhibition of COX-2 results in anti-inflammatory effects. [symbol: see text]Rofecoxib (Vioxx--MSD) and [symbol: see text]celecoxib (Celebrex--Searle) have been developed as selective inhibitors of COX-2. Rofecoxib is licensed for the symptomatic treatment of osteoarthritis, but not for rheumatoid arthritis. The manufacturer claims that "in clinical studies rofecoxib inhibits COX-2 but not COX-1", has "the power of high-dose NSAIDs--diclofenac and ibuprofen" and "superior GI safety profile compared to conventional NSAIDs". Celecoxib is licensed for symptom relief in osteoarthritis and rheumatoid arthritis. The manufacturer claims that celecoxib has "comparable efficacy and superior GI tolerability when compared to diclofenac or naproxen". Here, we review rofecoxib and celecoxib and consider whether they are safer than conventional NSAIDs.

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Colorectal cancer (CRC) is one of the most common neoplasia in Western countries and the second leading cause of cancer-related death. The vast majority of cases belong to sporadic forms, whereas a small but relevant proportion of them corresponds to inherited disorders, i.e. familial adenomatous polyposis and Lynch syndrome. These individuals with germline mutations in cancer-promoting genes, along with those who had already developed a colorectal neoplasm, either adenoma or carcinoma, stand to benefit from chemopreventive interventions. A large body of evidence indicates that the use of aspirin and other non-steroidal anti-inflammatory drugs (NSAID) can reduce the risk of CRC. Experimental studies have demonstrated that these drugs decrease the incidence of carcinogen-induced colon tumors in rodents, and several epidemiological investigations and therapeutic trials have also shown a 40-50% reduction in the risk of colorectal adenoma and cancer in individuals taking NSAIDs. Moreover, patients with familial adenomatous polyposis taking sulindac or celecoxib experience a reduction in adenoma size and number. The chemopreventive effects of NSAID are largely related to inhibition of cyclooxygenase-2 (COX-2), the inducible isoform of cyclooxygenase that catalyzes the conversion of arachidonic acid to prostaglandins. COX-2 overexpression is a frequent, but not universal event in colorectal neoplasms. Indeed, approximately 50% of adenomas and 80% of CRC express high levels of COX-2 mRNA and protein in neoplastic tissue. In this article, we will review the role of cyclooxygenase as a target for CRC chemoprevention, with special attention to the use of selective and non-selective COX-2 inhibitors in both individuals genetically predisposed and those who have already developed a colorectal neoplasm.

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Rats were administered either vehicle (VEH) (methylcellulose solution), blank NP, 40 mg/kg CEL in methylcellulose, or an equivalent NP dose (CEL-NP). Plasma and urine (over 12 hrs) samples were collected prior to and post-treatment. The mean percent change from baseline of urine flow rate along with electrolyte concentrations in plasma and urine were assessed based on 100 g body weight. Using tissues collected 24 hrs post-treatment, gastrointestinal inflammation was estimated through duodenal and gastric prostaglandin E2 (PGE2) and duodenal myeloperoxidase (MPO) levels; while kidney tissue was examined for dilatation and necrosis. CEL concentration was assayed in renal tissue and plasma utilizing high-performance liquid chromatography.

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Systemic hemodynamic function, including the response to COX2 inhibition, is related to filtration status in diabetic subjects and may reflect general endothelial dysfunction.

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Data were collected on 2846 patients; 1164 (41%) were taking NSAIDs (791 NSNSAIDs, 373 COX-2). Of the 1164 NSAID users, 753 (65%) had a diagnosis of RA or OA (483 NSNSAIDs, 270 COX-2). Overall, 37% of NSAID prescriptions were appropriate. Of the NSNSAID users, 92% had at least one risk factor for adverse gastrointestinal events and were therefore inappropriately treated. Prolonged use (in 89%) and age > or =65 yr (in 23%) were the most frequent risk factors identified. Of the COX-2 users, 97% had one or more risk factors and were appropriately treated. Analysis of the RA/OA subgroup revealed similar findings. Thirty-six per cent were taking NSAIDs appropriately; 97% of NSNSAID use was inappropriate and 97% of COX-2 use was appropriate treatment. In the whole cohort, gastroprotective agents were used in 26% of NSNSAID users, 56% of gastroprotective agents being proton pump inhibitors.

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A total of 36,354 patients (33.9%) claimed at least 1 prescription of an NSAID after discharge; 60,974 (56.9%) died, and 8970 (8.4%) and 39,984 (37.5%) were hospitalized with myocardial infarction or HF, respectively. The hazard ratio (95% confidence interval) for death was 1.70 (1.58-1.82), 1.75 (1.63-1.88), 1.31 (1.25-1.37), 2.08 (1.95-2.21), 1.22 (1.07-1.39), and 1.28 (1.21-1.35) for rofecoxib, celecoxib, ibuprofen, diclofenac, naproxen, and other NSAIDs, respectively. Furthermore, there was a dose-dependent increase in risk of death and increased risk of hospitalization because of myocardial infarction and HF. Propensity-based risk-stratified analysis and case-crossover models yielded similar results.

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celebrex 200 mg 2017-06-26

Cytokeratin 19 and its soluble fragment buy celebrex CYFRA have been studied as markers that may be associated with response to therapy and survival in non-small-cell lung cancer (NSCLC). As a prospective correlative study of Cancer and Leukemia Group B 30203, a randomized phase II trial of carboplatin/gemcitabine with eicosanoid modulators (celecoxib, zileuton, or both) in advanced NSCLC, serum CYFRA levels were obtained before and during treatment.

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Peak plasma concentrations (1234 +/- 528 microg/L) were buy celebrex achieved 3 hours after drug administration. The area under the celecoxib plasma concentration-time curve was 7709 +/- 3176 microg/L x h, the elimination half-life (t(1/2)) was 3.7 +/- 1.1 hours, the apparent volume of distribution was 7.9 +/- 7.8 L/kg, and the lower oral clearance of the drug was 1.4 +/- 1.0 L x h(-1) x kg(-1). Statistical analysis revealed a significantly lower [corrected] apparent oral clearance and longer t(1/2) (P <.05) at steady state compared with pharmacokinetics after a single dose. In addition, when the results were compared in children and adults, the drug was cleared approximately twice as fast in children and had a t(1/2) that was approximately half as long.

celebrex with alcohol 2016-01-14

Nonsteroidal anti-inflammatory drugs (NSAIDs) inhibit the formation of bone. However, they have been shown to increase tensile strength in healing tendons. Most NSAIDs inhibit two isoforms of cyclooxygenases called Cox-1 and Cox-2. Thanks to fewer side-effects, the recently introduced selective cyclooxygenase-2 (Cox-2) inhibitors will probably promote more widespread use of this kind of drug. To clarify the effects on tendon healing of a general Cox-inhibitor (indomethacin) as well as a selective Cox-2 inhibitor (celecoxib), we resected 3 mm of the Achilles tendon in rats and measured the strength of the tendon regenerate. Indomethacin given as daily injections in doses of 1.5, 3.0 and 5.0 mg/kg reduced the thickness (cross-sectional area) of the tendon regenerate at 14 days, as compared to controls, but there was no difference in the failure load or stiffness. In another series of measurements, indomethacin in a dose of 3.0 mg/kg reduced the cross-sectional area at 10, 14 and 18 days after transsection. Failure load was not affected, but tensile stress at failure was increased by indomethacin at 14 and 18 days. Indomethacin (3 mg/kg) was then compared to celecoxib (4.5 buy celebrex mg/kg) and controls 14 days after tendon transsection. No difference between the drugs was seen. Again, the transverse area was smaller in the treated tendons than in the controls. Failure load was unchanged and the tensile stress was higher in the treated tendons than in the controls. Because of the reduction in cross-sectional area without an effect on failure load, the use of Cox-inhibitors may be beneficial in clinical situations where thickening of a healing tendon is a problem--e.g., in the hand or shoulder.

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These results suggest that endogenous PGs derived from COX-1 play a crucial role in gastric mucosal defense during CRS, and this action is mainly mediated by PGI2 /IP receptors and partly buy celebrex by PGE2 /EP4 receptors.

celebrex dosage osteoarthritis 2015-02-22

There are currently no convincing data to support a benefit buy celebrex for NSAIDs in the treatment of CIN (very low quality evidence according to GRADE criteria). Results from a large on-going randomised study of celecoxib are awaited.

celebrex similar drugs 2017-08-13

The purpose of this study was to examine the effect of acute low-dose celecoxib administration on exercise-induced inflammation, muscle damage and lipid peroxidation. Twenty healthy untrained males (age: 25.5±4.5 yrs, weight: 72.7±7.9 kg, height: 177.3±7.2 cm) were randomly assigned to treatment (T) or placebo (P) groups. Blood samples were obtained before, immediately after, 3 h after and 24 h after exercise. Subjects ran for 30 min at 75% [Formula: see text]O2 max on a treadmill. Participants consumed 100 mg celecoxib or a placebo immediately after and 12 h after the immediately post-exercise blood sample. Total leukocytes, neutrophils, creatine kinase (CK), C-reactive protein (CRP) and malondialdehyde (MDA) were assessed at each time point. Significant increases in total leukocytes and neutrophils were observed 3 h after exercise in both groups (P < 0.05). CK and CRP levels were significantly increased immediately, 3 h and 24 h after exercise in both groups (P < 0.05). A significant increase in MDA was observed immediately after exercise in both groups (P < 0.05); however, no significant group differences were observed for MDA or CK. These findings suggest that inhibition of cyclo-oxygenase activity with low- buy celebrex dose celecoxib does not affect exercise-induced inflammation, muscle damage, or lipid peroxidation.

t celebrex dosage 2017-06-28

To determine whether U50488H, a selective agonist of kappa-opioid receptor, could induce biphasic (early and buy celebrex late) cardioprotection against myocardial ischemia/reperfusion injury and to explore the underlying mechanisms.

celebrex vs generic 2016-02-25

Patients with unresectable malignant pleural mesothelioma (MPM) received two intrapleural doses of a replication-defective adenoviral vector containing the human IFNα2b gene (Ad.IFN) concomitant with a 14- buy celebrex day course of celecoxib followed by chemotherapy. Primary outcomes were safety, toxicity, and objective response rate; secondary outcomes included progression-free and overall survival. Biocorrelates on blood and tumor were measured.

celebrex tab 2015-04-10

The compounds under study affect several pathways involved in cachexia by modulating inflammatory activity, anabolic potential, digestion and direct interaction with the muscle. Due to the multifactorial aspects of cachexia syndrome, combinations of these new drugs with nutritional intervention is probably the most promising approach. Furthermore, future studies should include interventions in pre-cachetic patients, as this stage might be more responsive to treatment. Future studies will benefit from well-defined end points and buy celebrex improved measures of cachexia, providing new insight into the disease. This insight, in combination with the elucidation of cachexia's underlying mechanism, will yield new treatment strategies in the near future.

celebrex and alcohol 2016-01-05

The multimodal use of the specific COX-2 inhibitor celecoxib in the postoperative period of orthopaedic procedures clearly improves postoperative pain, reduces the opioid consumption, releases the sleep disturbance, demonstrates more buy celebrex satisfaction in patients and lower chronic pain rate after discharge, without affecting the platelet and coagulation function.

celebrex loading dose 2017-06-29

In total 70236 patients (42 % males, 58 % females, mean age 60.3 years) were assessed. About 87 % of the patients were adequately treated with a daily dose of 200 mg. The tolerability of the treatment was judged to be "good" to "very good" by the physicians in 97 % and by buy celebrex the patients in 96 % of the cases. The overall incidence of undesirable events (UE) with or without potential causal relationship with the study medication was 2.8 % (1,955 patients), severe UEs manifesting in 0.3 % (223) of all patients.

celebrex brand name 2015-05-23

These results suggest that risk to buy celebrex the fetus should be carefully considered before administration of NSAIDs (especially systemic formulations, but including dermatological formulations) to women in the third trimester of pregnancy.

celebrex medicine 2016-05-14

Patients with familial adenomatous polyposis Zoloft User Reviews have a nearly 100 percent risk of colorectal cancer. In this disease, the chemopreventive effects of nonsteroidal antiinflammatory drugs may be related to their inhibition of cyclooxygenase-2.

celebrex maximum dosage 2017-03-11

A total of 52 outpatients with breast cancer with mild to moderate depression, who suffered from pain and needed analgesics, participated in the trial and underwent 6 weeks of treatment with either celecoxib (200 mg Ventolin Tabs twice daily) or diclofenac (50 mg twice daily). Participants were investigated using the Hamilton Depression Rating Scale (HDRS). The primary outcome measure was to compare the antidepressant effects of celecoxib and diclofenac.

celebrex cost australia 2017-12-04

Results from the present study clearly indicate that celecoxib exerts its anticancer effect partly Cymbalta Medication Uses through COX-2-independent mechanisms in addition to the known primary function of COX-2 inhibition.

celebrex 200mg generic 2017-03-15

Both traditional NSAIDs and coxibs compromise the glomerular filtration rate Claritin 60 Tablets in patients at increased risk. If there are differences in the blood pressure-raising potential of these drugs, these differences do not appear to be clinically significant.

celebrex 600 mg 2017-01-01

WIN-34B showed no signs of acute or chronic toxicity in terms of general behavior, gross appearance of the internal organs, blood chemistry, or mortality. WIN-34B did not cause significant gastric mucosal damage after single or repeated doses. In contrast, diclofenac and celecoxib both caused gastric damage. In terms of eicosanoid synthesis, WIN-34B significantly suppressed LTB(4) synthesis while both diclofenac and celecoxib increased LTB(4) synthesis. WIN-34B slightly reduced PGE(2) production, while both diclofenac and celecoxib significantly reduced PGE(2) production. In a rat model of diclofenac-induced gastric injury, WIN-34B significantly suppressed LTB(4) synthesis and restored PGE(2) Lopid 10 Mg release.

celebrex type drugs 2015-07-12

Excessive activation of TLR may induce endotoxin shock and inflammatory diseases, so the negative regulation of TLR-triggered inflammatory response attracts much attention. Nonpathogenic immune complex (IC) and Ig (IC/Ig) have been shown to play important roles in the regulation of immune responses and to be therapeutic in some kinds of autoimmune diseases. However, the role of IC/Ig in the regulation of TLR-triggered inflammatory responses and the underlying mechanisms remain to be fully understood. In this study we demonstrate that IC/Ig can significantly inhibit LPS-induced secretion of TNF-alpha and IL-6 from macrophages by preferentially inducing PGE(2). Pretreatment of mice with IC can protect wild-type mice, but not Fc gammaRIIb(-/-) mice, from lethal endotoxin shock, and significantly reduce the levels of serum TNF-alpha and IL-6 in wild-type mice but not in Fc gammaR IIb(-/-) mice. Furthermore, blockade of PGE(2) by celecoxib restores LPS-induced production of TNF-alpha and IL-6 in the presence of IC both in vitro and in vivo. Accordingly, blockade of PGE(2) production in vivo results in the increased sensitivity of IC-pretreated mice to lethal endotoxin shock. Therefore, IC/Ig can negatively regulate TLR4-triggered inflammatory response in macrophages through Fc gammaRIIb-dependent PGE(2). In addition, our results suggest that down-regulation of NF-kappaB activation and TLR4 expression but activation of protein kinase A pathway in macrophages by IC/Ig contribute to the negative regulatory process. Thus Duphaston Tab we provide new manner for the immune regulation and mechanistic explanation for nonpathogenic IC/Ig in the treatment of inflammatory or autoimmune diseases.

celebrex online 2016-10-09

To investigate the role of COX-2 inhibitor celecoxib in enhancing the lethal effects of Clomid Pills Pct bleomycin in Tca8113 cell line.

celebrex dosing 2017-11-03

PRA was high prior to drug administration, indicating slight salt depletion, and dropped by 65% after intake of celecoxib alone (p = 0.008) but only by 25% after combined Prograf 25 Mg intake with irbesartan (p = n.s.). GFR was not affected either by celecoxib alone or by combined administration with irbesartan. In contrast, ERPF increased by 28% 80 minutes after simultaneous drug intake (p = 0.029), but not after celecoxib alone. Renal sodium and potassium excretion did not significantly change under celecoxib alone or in combination with irbesartan.

celebrex highest dosage 2015-12-17

With a lower efficacy than Sou-Medrol in decreasing postoperative inflammation, celecoxib produces a better effect in inhibiting COX-2 expression, but it Cytoxan Tablets does not lower postoperative recurrence rate of rectal cancer.

celebrex reviews 2015 2017-04-28

Normal rat enterocytes (IEC18 cells) and their Ras-transformed derivatives (R1) were exposed for 72 h or over 6 months to celecoxib and analyzed for gene expression pattern using Genechip (RG-U34). Cluster and pathway analyses were done using GeneSpring software and Gene Ontology database. Cyclin Urispas Tablet Rate D1 was overexpressed in IEC18 cells using stable transfection; cell cycle and prostaglandin synthesis were assessed.

celebrex reviews 2017-04-13

To determine the efficacy of opioids in adults with CLBP.

celebrex cost comparison 2016-12-20

Polymethacrylates such as Eudragit® polymers are well established as drug delivery matrix. Here, we synthesize several Eudragit E PO (n-butyl-, dimethylaminoethyl-, methyl-methacrylate-terpolymer) analogues via free radical polymerization. These polymers are processed via hot melt extrusion, followed by injection molding and evaluated as carriers to produce immediate release solid solution tablets. Three chemical modifications increased the glass transition temperature of the polymer: (a) substitution of n-butyl by t-butyl groups, (b) reduction of the dimethylaminoethyl methacrylate (DMAEMA) content, and (c) incorporation of a bulky isobornyl repeating unit. These structural modifications revealed the possibility to increase the mechanical stability of the tablets via altering the polymer Tg without influencing the drug release characteristics and glassy solid solution forming properties. The presence of DMAEMA units proved to be crucial with respect to API/polymer interaction (essential in creating glassy solid solutions) and drug release characteristics. Moreover, these chemical modifications accentuate the need for a more rational design of (methacrylate) polymer matrix excipients for drug formulation via hot melt extrusion and injection molding.

celebrex medication 2017-07-05

It is unlikely that Celecoxib increases the risk of loosening, and it may be used safely in conjunction with TKR.

celebrex dosage medscape 2016-03-24

Previous studies have demonstrated that fatty acid amide hydrolase, the enzyme responsible for the metabolism of anandamide, is inhibited by the acidic non-steroidal anti-inflammatory drug (NSAID) ibuprofen with a potency that increases as the assay pH is reduced. Here we show that (R)-, (S)- and (R,S)-flurbiprofen, indomethacin and niflumic acid show similar pH-dependent shifts in potency to that seen with ibuprofen. Thus, (S)-flurbiprofen inhibited 2 microM [3H]anandamide metabolism with IC50 values of 13 and 50 microM at assay pH values of 6 and 8, respectively. In contrast, the neutral compound celecoxib was a weak fatty acid amide hydrolase inhibitor and showed no pH dependency (IC50 values approximately 300 microM at both assay pH). The cyclooxygenase-2-selective inhibitors nimesulide and SC-58125 did not inhibit fatty acid amide hydrolase activity at either pH. The data are consistent with the conclusion that the non-ionised forms of the acidic NSAIDs are responsible for the inhibition of fatty acid amide hydrolase.

celebrex generic name 2016-09-19

In spite of the proven efficacy of pharmacological prophylaxis of heterotopic ossification following total hip arthroplasty, its routine use is still debated, and no data are available regarding the adherence to its administration in clinical practice.

celebrex 200mg reviews 2015-11-03

The extent and severity of postoperative adhesions were significantly reduced in nimesulide group compared with the control group. The extent but not severity of adhesions in rats given indomethacin was significantly reduced. Celecoxib showed no significant reduction in the extent and severity of adhesions.

celebrex renal dosing 2017-06-07

We evaluated the incidence of acute toxicity of concurrent cyclooxygenase-2 inhibitor (celecoxib) plus radiotherapy in patients with locoregionally advanced nasopharyngeal carcinoma (NPC). Thirty-four patients received an accumulated radiation dose of 72-76Gy in 36-38 fractions to the primary lesion and 60Gy in 30 fractions to cervical lymph-node lesions. Palpable residual nodes were boosted to 70Gy at the 90% isodose level with an electron field. Celecoxib was administered at escalating doses of 400, 600, and 800mg/day, starting 3days before the first fraction of radiotherapy and continuing throughout the course of radiotherapy. The majority of toxicities were grade 1, with mucositis and weight loss most frequently observed (28 of 34, 82.4%), followed by dermatitis (27 of 34, 79.4%) and otitis (14 of 34, 41.2%). The toxicities were not related to celecoxib dose (all P>0.05). Stomach pain was considered related to celecoxib, which developed in 2 patients at doses of 400mg and 800mg/day. No grade-3 or -4 toxicities or episodes of toxic death occurred. The tumors in 31 patients (31/34, 91.2%) showed a complete response, and 3 patients (3/34, 8.8%) had partial responses. The actuarial local progression-free survival was 96.6% at 1year, and the 2year overall survival rate was 84.6%. Celecoxib can be safely administered concurrently with nasopharyngeal radiotherapy at doses up to 800mg/day. The tumors responded well to treatment warranting further assessment in a phase II trial.