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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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To evaluate the efficacy and potency of clinically available celecoxib for inhibition of ureteral contractility and prostanoid release. We have previously reported that the selective cyclooxygenase (COX)-2 inhibitor NS-398 inhibits ureteral contractility.

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A total of 170 nulliparous women who gave birth vaginally with episiotomy between March 2009 and November 2010 were randomly assigned to receive either ibuprofen or celecoxib which were given orally every 6 or 12 hours, respectively. Pain levels were measured before the intervention, and at 1, 2, 4, 8 and 12 hours after providing the first dose on a 10-cm visual analogue scale.

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In comparison with historically reported response rates, these data suggest that the addition of a selective COX-2 inhibitor may enhance the response to preoperative paclitaxel and carboplatin in patients with NSCLC. Moreover, treatment with celecoxib 400 mg twice daily was sufficient to normalize the increase in PGE2 levels found in NSCLC patients after treatment with paclitaxel and carboplatin. Confirmatory trials are planned.

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

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To assess the overall and progression-free survival, response rate, and toxicity of combined docetaxel and celecoxib in the treatment of patients with non-small cell lung cancer progressing after initial chemotherapy for advanced disease.

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Prostaglandins (PGs), particularly PGE2 and PGI2, have a salutary effect on myocardial ischemia-reperfusion-induced myocardial damage.

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Low-dose cyclophosphamide, methotrexate and high-dose celecoxib are well tolerated and active in pre-treated diffuse large cell B lymphoma. Although thrombotic events were not observed during this study, close surveillance for arterial and venous thrombotic events is recommended.

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The cardiovascular safety of nonsteroidal antiinflammatory drugs (NSAIDs) may be influenced by interactions with antiplatelet doses of aspirin. We sought to quantitate precisely the propensity of commonly consumed NSAIDs—ibuprofen, naproxen, and celecoxib—to cause a drug-drug interaction with aspirin in vivo by measuring the target engagement of aspirin directly by MS. We developed a novel assay of cyclooxygenase-1 (COX-1) acetylation in platelets isolated from volunteers who were administered aspirin and used conventional and microfluidic assays to evaluate platelet function. Although ibuprofen, naproxen, and celecoxib all had the potential to compete with the access of aspirin to the substrate binding channel of COX-1 in vitro, exposure of volunteers to a single therapeutic dose of each NSAID followed by 325 mg aspirin revealed a potent drug-drug interaction between ibuprofen and aspirin and between naproxen and aspirin but not between celecoxib and aspirin. The imprecision of estimates of aspirin consumption and the differential impact on the ability of aspirin to inactivate platelet COX-1 will confound head-to-head comparisons of distinct NSAIDs in ongoing clinical studies designed to measure their cardiovascular risk.

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Potential under utilization of GIPT in this subject population was more prevalent than potential overutilization of GIPT. Although all hypothesized risk factors were significantly associated with receiving GIPT, physician education on GI risk factors might improve prescribing of GIPT for elderly persons in Nova Scotia.

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Medulloblastomas are the most common malignant brain tumors in children. They express high levels of COX-2 and produce PGE2, which stimulates tumor cell proliferation. Human cytomegalovirus (HCMV) is prevalent in the human population and encodes proteins that provide immune evasion strategies and promote oncogenic transformation and oncomodulation. In particular, HCMV induces COX-2 expression; STAT3 phosphorylation; production of PGE2, vascular endothelial growth factor, and IL-6; and tumor formation in vivo. Here, we show that a large proportion of primary medulloblastomas and medulloblastoma cell lines are infected with HCMV and that COX-2 expression, along with PGE2 levels, in tumors is directly modulated by the virus. Our analysis indicated that both HCMV immediate-early proteins and late proteins are expressed in the majority of primary medulloblastomas. Remarkably, all of the human medulloblastoma cell lines that we analyzed contained HCMV DNA and RNA and expressed HCMV proteins at various levels in vitro. When engrafted into immunocompromised mice, human medulloblastoma cells induced expression of HCMV proteins. HCMV and COX-2 expression correlated in primary tumors, cell lines, and medulloblastoma xenografts. The antiviral drug valganciclovir and the specific COX-2 inhibitor celecoxib prevented HCMV replication in vitro and inhibited PGE2 production and reduced medulloblastoma tumor cell growth both in vitro and in vivo. Ganciclovir did not affect the growth of HCMV-negative tumor cell lines. These findings imply an important role for HCMV in medulloblastoma and suggest HCMV as a novel therapeutic target for this tumor.

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An increasing number of patients with advanced pancreatic or biliary tract cancer who progress after a gemcitabine-containing regimen are candidates for further chemotherapy. We therefore evaluated a fully oral regimen of capecitabine and celecoxib (CapCel) as second-line treatment in these patients.

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Oxaliplatin (OXA) is the common and extremely potent anti-advanced colorectal cancer chemotherapeutic. Accumulating evidence reveals that OXA evokes mechanical and cold hypersensitivity. However, the mechanism underlying these bothersome and dose-limiting adverse effects is poorly understood. It is well known that cyclooxygenase-2 (COX-2) as well as phosphoinositide 3-kinase (PI3K)/Akt signaling mediate the neuropathic pain. But it is still unclear whether COX-2 or PI3K/Akt signaling participates in the regulation of OXA-induced hypersensitivity, as well as the linkage between COX-2 and PI3K/Akt signaling in mediating OXA-induced hypersensitivity. In this paper, we investigated the anti-nociceptive effect of celecoxib, an inhibitor of COX-2, on the OXA-induced neuropathic pain. We found that OXA increased the expression of cyclooxygenase-2 (COX-2) and Akt2 in the lumbar 4-5 (L4-5) dorsal root ganglion (DRG). And the administration of celecoxib alleviates the OXA-induced hypersensitivity and suppresses the COX-2 and PI3K/Akt2 signaling. Our findings showed that COX-2 and PI3K/Akt2 signaling in DRG contributed to the OXA-induced neuropathic pain. In addition, celecoxib enhanced the OXA-induced mortality of the human colon cancer cell line HCT-116. Thus, celecoxib might play a dual role in colorectal cancer treatment: alleviating OXA-induced neuropathic pain and facilitating the anti-tumor effects of OXA through their synergistic role.

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Chronic myelogenous leukemia is a neoplasm of myeloid progenitor cells. We recently found that rapamycin could induce G0/G1 phase arrest and apoptosis and inhibit proliferation of K562 cells through inhibiting mammalian target of rapamycin (mTOR) pathway. However, whether rapamycin has synergistic effects with other drugs in chronic myelogenous leukemia (CML) therapies remain unclear. Therefore, we examined the effect of rapamycin combined with celecoxib on K562 cells in vitro. The survival rates showed a significant decrease in rapamycin + celecoxib treatment group. The combination treatment also increased the G0/G1 phase cells as compared to rapamycin or celecoxib treatment alone (P < 0.05), accompanied with the decreased population of S phase cells. Meanwhile, the rate of apoptosis was 15.87 ± 2.21 % in rapamycin + celecoxib treatment group, significantly higher than that in mono treatment group (P < 0.05). Western blot and reverse transcription PCR (RT-PCR) analysis showed that the expressions of mTOR, 4E-BP1, and p70S6K were all significantly decreased in K562 cells after rapamycin + celecoxib treatment (P < 0.05). In conclusion, rapamycin combined with celecoxib could induce cell cycle arrest and apoptosis and decrease the expressions of mTOR, 4E-BP1, and p70S6K. It suggested that the combination could enhance the antitumor effects of mono treatment on CML cells through downregulating mTOR pathway.

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Among the 50,087 "serious" ADRs registered in the database during this period, 1,127 were thrombotic ones. Rofecoxib exposure was significantly associated with high values of odds ratio (OR) [4.2 (95% CI 1.97-8.61)] for thrombotic ADRs as early as the end of 2001. The values of ADR reporting ORs remained high (3.0-3.5) until 2006. For celecoxib, a significant trend occurred only from September 2004.

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Only one hypersensitivity reaction to CE was documented among 29 P-intolerant patients. Thus, we conclude that CE is a reasonably safe alternative which can be used in subjects who do not tolerate P.

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To determine the milk-to-plasma (M/P) concentration ratio of celecoxib, and estimate likely infant exposure.

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We conducted a population-based matched case-control study over the years 2000-3 in outpatient residents of Finland. In the nationwide Hospital Discharge Register 33 309 persons with first time MI were identified. A total of 138 949 controls individually matched for age, gender, hospital catchment area, and index day were selected from the Population Register. For combined NSAIDs, the adjusted odds ratio for the risk of first MI with current use was 1.40 (95% CI, 1.33-1.48). The risk was similar for conventional (1.34; 1.26-1.43), semi-selective (etodolac, nabumetone, nimesulide, and meloxicam) (1.50; 1.32-1.71), and cyclo-oxygenase-2 (COX-2) selective NSAIDs (rofecoxib, celecoxib, valdecoxib, and etoricoxib) (1.31; 1.13-1.50). Age of current user did not consistently modify the risk. No NSAID was associated with an MI-protective effect. All durations from 1 to 180 days of conventional NSAIDs and from 31 to 90 days duration of COX-2 selective NSAIDs were associated with an elevated risk of MI.

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The expression of the putative markers LGR-5 (leucine-rich-repeat-containing G-protein-coupled receptor 5), MSI-1 (Musashi-1) and DCAMKL-1 (doublecortin and calcium/calmodulin-dependent protein kinase-like-1) was studied in normal colon mucosa (NM), in the precancerous lesions Mucin Depleted Foci (MDF) and in macroscopic tumours (adenomas) of 1,2-dimethylhydrazine-treated rats. Co-localization between these markers and nuclear β-catenin (NBC), an attributed feature of cancer stem cells, was also determined. Moreover, since PGE2 could increase NBC, we tested whether short-term treatment with celecoxib, a COX-2 inhibitor (2 weeks, 250 ppm in the diet) could reduce the expression of these markers.

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Malignant mesothelioma (MM) is a rare neoplasm that is commonly fatal within 12-17 months after diagnosis. There are no widely accepted curative approaches. It recurs even after the most aggressive surgical resection. MM is resistant to chemotherapy and radiation. Most of the chemotherapeutics have been evaluated in MM, however, no drugs have a response rate greater than 20%. The combination of drugs has no increased efficacy compared with single agents. Vinorelbine has useful clinical activity against MM with a response rate of 24%. Vascular endothelial growth factor (VEGF) is expressed in MM and pleural effusion of MM. There is a significant inverse correlation between serum VEGF levels and MM patient survival. Cyclooxygenase-2 (COX-2) is expressed in MM. COX-2 plays an important role in tumor growth, invasion, and angiogenesis. VEGF and COX-2 are potential targets in MM. The downregulation of bFGF, VEGF, and maybe some other angiogenesis stimulators, is one of the antiangiogenic mechanisms of thalidomide. Celecoxib is a potent selective COX-2 inhibitor. Here we report a case of disseminated malignant mesothelioma of peritoneum responding remarkably to thalidomide, celecoxib, vinorelbine and CDDP.

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The pharmacokinetics of celecoxib, a cyclooxygenase-2 inhibitor, was characterized in beagle dogs. Celecoxib is extensively metabolized by dogs to a hydroxymethyl metabolite with subsequent oxidization to the carboxylic acid analog. There are at least two populations of dogs, distinguished by their capacity to eliminate celecoxib from plasma at either a fast or a slow rate after i.v. administration. Within a population of 242 animals, 45.0% were of the EM phenotype, 53.5% were of the PM phenotype, and 1.65% could not be adequately characterized. The mean (+/-S.D.) plasma elimination half-life and clearance of celecoxib were 1.72 +/- 0.79 h and 18.2 +/- 6.4 ml/min/kg for EM dogs and 5.18 +/- 1.29 h and 7.15 +/- 1.41 ml/min/kg for PM dogs. Hepatic microsomes from EM dogs metabolized celecoxib at a higher rate than microsomes from PM dogs. The cDNA for canine cytochrome P-450 (CYP) enzymes, CYP2B11, CYP2C21, CYP2D15, and CYP3A12 were cloned and expressed in sf 9 insect cells. Three new variants of CYP2D15 as well as a novel variant of CYP3A12 were identified. Canine rCYP2D15 and its variants, but not CYP2B11, CYP2C21, and CYP3A12, readily metabolized celecoxib. Quinidine (a specific CYP2D inhibitor) prevented celecoxib metabolism in dog hepatic microsomes, providing evidence of a predominant role for the CYP2D subfamily in canine celecoxib metabolism. However, the lack of a correlation between celecoxib and bufuralol metabolism in hepatic EM or PM microsomes indicates that other CYP subfamilies besides CYP2D may contribute to the polymorphism in canine celecoxib metabolism.

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To undertake a systematic review and meta-analysis of controlled observational studies to compare the risks of serious cardiovascular events with individual NSAIDs and cyclooxygenase 2 inhibitors.

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Cancer chemoprevention is a new approach in the management of cancer. Traditional cytotoxic chemotherapeutic approaches cannot cure most advanced solid malignancies. Chemoprevention can be defined as the use of non-cytotoxic drugs and natural agents to block the progression to invasive cancer. Chemoprevention can either prevent DNA damage that initiates the neoplastic transformation process or reverses the progression of pre-invasive lesions. Epidemiological observations, experimental evidence from animal carcinogenesis models, knock-out models, cancer cell lines and clinical trials have shown the efficacy of this approach. Recent advances in our understanding of carcinogenesis have led to the synthesis of new drugs that target specific receptors. Non-steroidal anti-inflammatory drugs target the prostaglandin pathway. The identification of the role of cyclooxygenase-2 in epithelial carcinogenesis led to the synthesis of selective cyclooxygenase-2 inhibitors (Celecoxib). Celecoxib was subsequently approved for the prevention of colon polyps in familial adenomatous polyposis after the completion of a randomized clinical trial. The large chemoprevention clinical trial with the selective estrogen receptor modulator, tamoxifen, showed the benefit of tamoxifen in the prevention of breast cancer in high-risk women. Retinoids and rexinoids target the retinoid receptors and have a role in chemoprevention of aerodigestive, hepatic and cervical neoplasia. Selenium, an inhibitor of the glutathione peroxidase system, is being tested in the chemoprevention of prostate cancer and lung cancer. The different isoforms of vitamin E (tocopherols) may be chemopreventive. Recent evidence indicates that gamma-tocopherol may be a more powerful chemopreventive than the alpha-tocopherol. The review details the rationale, experimental and clinical evidence and the drug targets of the chemopreventive agents that are currently in various phases of clinical development.

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celebrex user reviews 2015-08-05

These results suggest that celecoxib buy celebrex may play a role in modifying the natural history of hepatocellular carcinoma development.

celebrex reviews 2015 2017-07-04

We examined the involvement of adipocyte cyclooxygenase-2 (COX-2) and prostaglandin E2 (PGE2)-prostaglandin E receptor (EP)3-mediated signaling during hypertrophy and hypoxia in the development of obesity-associated adipose tissue (AT buy celebrex ) inflammation and insulin resistance. The experiments were conducted with high-fat diet (HFD)-induced obese rats, db/db mice, human subjects, and 3T3-L1 and the human Simpson-Golabi-Behmel syndrome (SGBS) adipocytes; the groups were treated with selective inhibitors of COX-2 [celecoxib 30 mg/kg, half maximal inhibitory concentration (IC50) ≈ 0.04 µM] and EP3 (L-798106 100 µg/kg, IC50 ≈ 0.5 µM) or a short interfering RNA. There were strong, positive correlations between adipocyte COX-2 and EP3 gene expressions and the AT TNF-α and monocyte chemotactic protein-1 contents and the homeostatic model assessment for insulin resistance in HFD-induced obese rats, as well as body mass index in human subjects. Treatment with COX-2 and EP3 inhibitors significantly reversed AT inflammatory gene and protein expressions (-50%) and impaired glucose and insulin tolerance in db/db mice. COX-2 inhibition diminished the chemotaxis of adipocytes isolated from HFD rats to macrophages and T cells. Targeting inhibition of adipocyte COX-2 and EP3 during hypertrophy and hypoxia reversed the release of the augmented proinflammatory adipokines and the diminished adiponectin and also suppressed NF-κB and hypoxia-inducible factor-1α transcription activation. These findings suggest that adipocyte COX-2 PGE2-EP3-mediated signaling is crucially involved in the development of obesity-associated AT inflammation and insulin resistance.-Chan, P.-C., Hsiao, F.-C., Chang, H.-M., Wabitsch, M., Hsieh, P. S. Importance of adipocyte cyclooxygenase-2 and prostaglandin E2-prostaglandin E receptor 3 signaling in the development of obesity-induced adipose tissue inflammation and insulin resistance.

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GW406381 10, 20, 35, or 50 mg, celecoxib buy celebrex 200 mg, or placebo. Study B: GW406381 1, 5, 10, 25, or 50 mg, celecoxib 200 mg, or placebo.

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The average age of the patients was 51.47 ± 11.49 years. The incidence of acute mucositis at the end of the 1st week was 33.3 buy celebrex % that was gradually increased until the end of the 5th week (93.3%) and then had a decreasing trend within the 6th week (70.0%). The incidence of acute dysphagia was estimated 23.3% at the end of the 1st week and reached 60% at completion of treatment.

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Chronic COX-2 inhibition attenuated progressive nephropathy by buy celebrex reducing glomerular hypertension, renal inflammation, and ectopic COX-2 expression, indicating a complex contribution of COX-2 to progressive renal injury in 5/6 nephrectomy rats.

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Celecoxib alone decreased the growth of prostate tumors mostly by inducing mitotic failure, which resulted in increased apoptosis. Surprisingly, celecoxib did not buy celebrex possess significant angiostatic activity. Surgical or chemical castration prevented the growth of prostate tumors and this, on the other hand, was associated with disruption of the tumor vasculature. Finally, androgen withdrawal combined with celecoxib caused tumor regression through decreased angiogenesis and increased mitosis arrest and apoptosis.

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The Glucosamine/chondroitin Arthritis Intervention Trial (GAIT) was a randomized double-blind placebo and active comparator (celecoxib) controlled trial of 1583 persons with symptomatic osteoarthritis (OA) of the knee(1). Patients randomized to celecoxib had significant improvement in knee pain compared to those randomized to placebo. No statistically significant improvement in knee pain compared to placebo was seen among patients randomized to the dietary supplements, although a subset of patients with moderate-to-severe knee pain at entry who were assigned to the combination of glucosamine and chondroitin sulfate did seem to experience some improvement. Additionally, patients buy celebrex taking chondroitin sulfate were noted to have a statistically significant improvement in knee joint swelling. An exploratory post hoc analysis of GAIT patients suggested the effect of chondroitin sulfate on joint swelling occurred more often in patients with milder pain and lower Kellgren-Lawrence Grade at entry.

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The results suggested that celecoxib displayed a multiple physiological function in a buy celebrex time-dependent manner.

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This is the fourth buy celebrex report in the English-language literature describing cholestatic hepatitis temporally related to celecoxib use, the second supported by histologic findings typical of drug-induced cholestasis, and the first in a patient who denied use of alcoholic beverages and was taking no other drugs or herbal products at the time of the reaction. The Naranjo probability scale indicated that celecoxib was a probable cause of acute cholestatic hepatitis in this patient.

celebrex normal dosage 2016-06-29

Lornoxicam exhibits strong analgesic but weak antipyretic effects in rats with paw inflammation. Such a separation of effects is related to its efficacy in the reduction of PGE2 levels in the paw and buy celebrex brain hypothalamus.

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RT-PCR showed that the expression COX-2 mRNA was strongly down-regulated in SKOV3 cells after treatment with Celecoxib or Aspirin. FCM and buy celebrex Western blot analysis showed that the protein product of COX-2 was strongly decreased by Celecoxib or Aspirin. The Celecoxib was more potential effects than Aspirin. The immunocytochemistry result showed that the expression of COX-2 in 10, 25, 50 mg/kg x d of Celecoxib were lower obviously than it in the control group in Xenografted nude mice.

celebrex usual dosage 2017-09-30

Treatment of malignant gliomas consists of resection followed by radiotherapy and chemotherapy. Celecoxib (CXB), a selective COX-2 inhibitor, is able to control inflammation and pain, to improve the efficacy of radiotherapy, and to inhibit at high doses the growth of cancer cells. Two new delivery systems for CXB are developed: microspheres (MPs) for implantation in the brain after partial/complete removal buy celebrex of the tumor, and nanoparticles (NPs) for their potential to cross the blood brain barrier and deliver CXB into the CNS. Cell culture assays performed in PC12, SKN-AS and U373-MG cells demonstrate the antiproliferative affects of CXB, with EC50 values of 99.81 μM and 82.4 μM in U373-MG and SKN-AS cells. Encapsulation efficacy of CXB in formulation MP2 (20% CXB) was 74.6 ± 2.2% with a zero-order release rate of 47.8 μg/day/20mg microspheres for 34 days. Uncoated and polysorbate 80-coated CXB-NPs are prepared by nanoprecipitation. Mean sizes of uncoated and coated CXB-NPs were 173.6 ± 44.9 nm and 100.6 ± 62.1 nm. Cerebral cortex images showed a marked increase of fluorescence when the surfactant-coated NPs were administered to rats. These results suggest that both CXB formulations (MPs and NPs) are adequate systems to enhance the effects of chemotherapy in the treatment of malignant brain tumor.

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Anti-nociceptive activities of WIN-34B (100, 200 and 400 buy celebrex mg/kg, p.o.) were measured using acetic acid-induced writhing response, formalin-induced paw licking, hot plate, radiant heat tail-flick, carrageenan-induced paw pressure, and Hargreaves tests, respectively. Anti-inflammatory activities of WIN-34B (100, 200 and 400 mg/kg, p.o.) were assessed using acetic acid-induced vascular permeability, carrageenan-induced paw edema, and croton oil-induced ear edema. Anti-osteoarthritis effect of WIN-34B was analyzed using monosodium iodoacetate (MIA)-induced osteoarthritis animal model.

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Prostacyclin (PGI(2)) is a vasodilator and platelet inhibitor, properties consistent with cardioprotection. More than a decade ago, inhibition of cyclooxygenase-2 (COX-2) by the nonsteroidal anti-inflammatory drugs (NSAIDs) rofecoxib and celecoxib was found to reduce the amount of the major metabolite of PGI(2) (PGI-M) in the urine of healthy volunteers. This suggested that NSAIDs might buy celebrex cause adverse cardiovascular events by reducing production of cardioprotective PGI(2). This prediction was based on the assumption that the concentration of PGI-M in urine likely reflected vascular production of PGI(2) and that other cardioprotective mediators, especially nitric oxide (NO), were not able to compensate for the loss of PGI(2). Subsequently, eight placebo-controlled clinical trials showed that NSAIDs that block COX-2 increase adverse cardiovascular events. We connect tissue-specific effects of NSAID action and functional correlates in mice with clinical outcomes in humans by showing that deletion of COX-2 in the mouse vasculature reduces excretion of PGI-M in urine and predisposes the animals to both hypertension and thrombosis. Furthermore, vascular disruption of COX-2 depressed expression of endothelial NO synthase and the consequent release and function of NO. Thus, suppression of PGI(2) formation resulting from deletion of vascular COX-2 is sufficient to explain the cardiovascular hazard from NSAIDs, which is likely to be augmented by secondary mechanisms such as suppression of NO production.

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This study shows that celecoxib is effective in improving locomotor function and pain in patients with Zyrtec Generic Target knee OA.

celebrex dosage medication 2017-08-04

These findings suggest that although inhibitors of COX-2 or COX-1 reduced PGE(2) synthesis, only the COX Effexor Generic Brands -2 enzyme plays a role in the mechanism of traumatic HO.

celebrex brand name 2017-03-28

Selective COX-2 inhibitors (COXib) belonging to the class of diaryl heterocycles (e.g., celecoxib, rofecoxib, etc.), are devoid of the undesirable effects due to their capacity to inhibit selectively inducible (COX-2), responsible for inflammatory effects but not constitutive cyclooxygenase-1 (COX-1)(COX); responsible for cytoprotective effects on gastric mucosa. In addition, several reports have identified an increased risk of cardiovascular events associated with the use of COXib. We have developed a new series of anti-inflammatory agents (1,5-diarylpyrrole-3-alkoxyethyl esters and ethers). To evaluate the effect Avelox 7 Tablets of two 1,5-diarylpyrrole-3-alkoxyethyl ethers, VA441 and VA428 (up to 100 μM), respectively, in comparison with two well known COXib, celecoxib and rofecoxib, on HaCaT cell (keratinocytes) proliferation and toxicity. Crucial molecules in cell cycle progression, i.e. NFκB and ERK as targets/mediators and cyclin D1 and p21 Cip1/Kip as final effectors were evaluated by Western blot, immunohystochemistry and q-PCR analysis. Both compounds, VA441 and VA428, showed a strong inhibition of cell proliferation, and did not exhibit cytotoxicity. The anti-proliferative effect was accompanied by a strong activation of ERK and induction of the cell cycle inhibitor p21. In addition, there was a clear inhibition of the transcription factor NF-κB and downregulation of cyclin D1, with enforced inhibition of the HaCaT cell cycle progression. These data suggest that compounds VA441 and VA428, along with their role in inhibiting COX-2 and inflammation, could have a possible therapeutic (topical and systemic) use against skin proliferative disorders, such as psoriasis.

celebrex 10 mg 2016-01-26

P-34 (expressing high levels of COX-2), and MIAPaCa (expressing low levels of COX-2) and Panc-1 (no expression of Cleocin Ovules Dosage COX-2) evaluated cell lines were exposed to different concentrations of celecoxib (0-40 microM), curcumin (0-20 microM) and their combination. Cell viability was by XTT assay. Apoptosis was assessed by flow cytometry and COX-2 expression was measured by Western blotting analysis.

celebrex replacement drugs 2017-05-21

The coadministration of placebo or celecoxib did not undermine the aspirin-related inhibition of platelet COX-1 activity, as assessed by measurements of serum thromboxane B(2) (TXB(2)) levels, as well as platelet function. In contrast, a significant (P < .001) increase in serum TXB(2) level was detected on day 7 before drug administration (median, 19.13 ng/mL [range, 1-47.5 ng/mL]) and at 24 hours after the coadministration of aspirin and ibuprofen (median, 22.28 ng/mL [range, 4.9-44.4 ng/mL]) versus baseline (median, 1.65 ng/mL [range, 0.55-79.8 ng/mL]); this was associated with a significant increase in arachidonic acid-induced platelet aggregation (P < .01) and adenosine diphosphate-induced platelet aggregation (P < .05) and a decrease in the time to form an occlusive thrombus in the platelet function analyzer (P < .01). The urinary Benicar Max Dosage excretion of 11-dehydro-TXB(2), an index of systemic thromboxane biosynthesis, was not significantly affected by the coadministration of treatment drugs. At steady state, a comparable and persistent inhibition of lipopolysaccharide-stimulated prostaglandin E(2) generation, a marker of COX-2 activity ex vivo, was caused by ibuprofen (>or=80%) or celecoxib (>or=70%) but not placebo.

celebrex generic cost 2015-11-11

(1) The 22nd French pharmacovigilance meeting, held in July 2001, presented data on adverse effects notified by health professionals to regional pharmacovigilance centres in France. (2) Non specific "immunostimulants" are not harmless placebos, as might be concluded from the relative lack of data. There have been 315 notifications of severe adverse effects, some with positive rechallenge, reporting cutaneous, gastrointestinal, respiratory, haematological and other disorders. Attributability was considered "likely" in 68% of cases. Three deaths occurred. (3) Other well known adverse effects continue to occur: convulsions with camphor, visual hallucinations with oxybutynin, headache with antimigraine drugs, liver damage with dextropropoxyphene, neuropsychological disorders after buflomedil overdose (especially in patients with renal failure), hyperkalaemia during spironolactone combination with an angiotensin-converting-enzyme inhibitor (ACE inhibitor), and severe infections after intravesical BCG. (4) Rare adverse effects of old drugs were identified, such as oedema with valproic acid, interstitial pneumonia with flecainide, and a bleeding risk due to tramadol interaction with oral anticoagulants Famvir Buy Online . (5) The adverse effects of new drugs are better documented: celecoxib is now implicated in visual disorders. (6) Overall, the meeting confirmed that only a small proportion of adverse drug reactions are notified, that a large number of hospitalised patients suffer from drug induced complications, and that summaries of product characteristics (SPC) are often too brief or reassuring regarding pharmacovigilance data. The poor risk-benefit ratios of some drugs call for their immediate market withdrawal.

celebrex dosage forms 2015-01-11

Hyperalgesia to mechanical stimuli was induced in rat hind paws by intraplantar injection of carrageenan and measured using the Randall-Selitto method over Amaryl Drug Class the next 8 hours. The effects of systemic pretreatment with celecoxib and a range of cytoskeletal disruptors (colchicine, nocodazole, cytochalasin B, latrunculin B, acrylamide, each given by intraplantar injection) on carrageenan-induced hyperalgesia were similarly investigated. Morphine and other selective cyclo-oxygenase 1 (SC-560), cyclo-oxygenase 2 (SC-236), and nonselective cyclo-oxygenase (indomethacin) inhibitors were also tested under similar conditions.

celebrex drug class 2015-11-16

(1) Concomitant use of a classical NSAID and a vitamin K antagonist carries a risk of bleeding. Some NSAIDs, and especially phenylbutazone Ceftin Uti Dosage , increase the INR. NSAIDs have antiplatelet effects and can cause gastrointestinal erosions and bleeding. (2) Celecoxib or rofecoxib in combination with an oral anticoagulant has been reported to increase the INR and, in some cases, to cause bleeding. The "coxibs" can also cause bleeding-prone gastrointestinal lesions. (3) If a coxib is combined with an oral anticoagulant then the INR must be watched closely.

celebrex similar drugs 2016-09-06

To evaluate the roles and mechanisms of celecoxib in inducing proliferation inhibition and apoptosis of human cholangiocarcinoma cell lines.

celebrex generic availability 2017-11-06

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.

celebrex dose form 2016-06-30

Recent preclinical as well as clinical trials have provided data on the potential benefit of a number of drugs and nutritional elements in the field of CRC prevention. Currently, only celecoxib is FDA approved for chemoprevention of CRC and only for high-risk patients with Familial Adenomatous Polyposis (FAP). This is mainly due to cardiovascular toxicity reported in individuals with a personal history of sporadic adenomas. Aspirin and sulindac have also repeatedly demonstrated efficacy in this setting. However, due to increased risk of associated GI toxicity their benefit will have to be weighed against their risk. Combination therapy, using lower doses of each medication, is drawing a great deal of attention and many studies utilizing a variety of chemopreventive agents are presently under study. Promising results have recently been published using sulindac and DFMO.

celebrex high dose 2017-07-04

This was a single-dose, 2-center, randomized, double-blind, active- and placebo-controlled study in which patients with moderate to severe pain following third molar extraction were randomized to receive a single dose of celecoxib 400 mg, ibuprofen 400 mg, or placebo. Pain assessments were completed using a 4-point pain intensity scale where 0=no pain and 3=severe pain and a 5-point pain relief scale where 0=no pain relief and 4= complete pain relief at baseline and 18 time points over 24 hours. Primary efficacy outcome measures were time to onset of analgesia (the median time to perceptible pain relief in those patients who achieved meaningful pain relief), time-specific pain intensity difference (PID), time-specific pain relief (PR), time-specific sum of PID and PR, and time to use of rescue medication. Times to perceptible and meaningful pain relief (secondary efficacy outcome measures) were recorded using 2 stopwatches. Tolerability was assessed through recording of adverse events, clinical laboratory tests, and physical examinations (including collection of vital signs).

celebrex 600 mg 2017-09-30

An observational study was undertaken in which the Department of Veterans' Affairs claims dataset was used to identify: veterans dispensed ACE inhibitors (ACEIs) or angiotensin II type 1 receptor antagonists (angiotensin receptor blockers [ARBs]) and furosemide (ACEI-ARB/furosemide cohort); veterans dispensed medicines for diabetes (diabetes cohort); and all other veterans (reference cohort) from July 1999 to July 2007. Concurrent dispensing of NSAIDs was assessed.

celebrex maximum dosage 2016-05-24

Chronic arthritis was induced in immunized rabbits by repeated intra-articular injections of ovalbumin. To increase the degree of systemic inflammation and also to induce atherosclerotic lesions, the animals were fed a hyperlipidaemic diet (2% cholesterol and 6% peanut oil) and were given an endothelial injury of the femoral artery. Rabbits were randomized to receive the COX-2 inhibitor celecoxib (10 mg·kg⁻¹ ·day⁻¹) or no treatment. After 4 weeks, sera, peripheral mononuclear cells and vessel specimens were collected.