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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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Tityus serrulatus venom (Tsv) was intraperitoneally (ip) injected at doses of 75, 150 and 300mug/kg and IL-1beta (2.0 microg/kg) was given intravenously (iv) to male Wistar rats. Rectal temperature was measured by radiotelemetry. Vagotomy was performed according to Bluthe et al. [1994. Lipopolysaccharide induces sickness behaviour in rats by a vagal mediated mechanism. C R Acad. Sci. 317(6), 499-503]. Cerebrospinal fluid (CSF) and peritoneal fluid (PF) levels of bradykinin (BK) were measured by ELISA. B(1) (des-Arg(9)-[Leu(8)]-BK; DALBK) and B(2) kinin receptor (icatibant) antagonists (1.0 mg/kg each), the induced nitric oxide synthase inhibitor aminoguanidine (50.0 mg/kg), the neuronal nitric oxide synthase inhibitor 7-nitroindazole (30.0 mg/kg), the dual cyclooxygenase inhibitor ibuprofen (10.0 mg/kg), the selective interleukin-1 receptor antagonist IL-ra (2.0 mg/kg) and dipyrone (120 mg/kg) were given ip. Celecoxib (5 mg/kg) was given per os (po). Tsv at doses of 75 microg/kg evoked no change in rectal temperature while at doses of 150 and 300 microg/kg it promoted long-lasting fever (2 degrees C+/-0.1). Tsv (150 microg/kg) increased by nearly 3 and 5 times, respectively BK concentration in the CSF and in the PF. Subdiaphragmatic vagotomy or 7-nitroindazole reduced, icatibant, DALBK, IL-1ra, aminoguanidine and dipyrone abolished, while ibuprofen and celecoxib failed to affect Tsv-induced fever. These results suggest that PGs do not play a relevant role, whereas, kinins via their B(1) and B(2) receptors, IL-1, nitric oxide and vagal neurotransmission are involved in Tsv-induced fever.

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Joint pain is the main complaint in patients affected by osteoarthritis (OA), and NSAIDs are commonly used to treat pain associated with OA. Over the past few years, cyclo-oxygenase (COX)-2-selective inhibitors have been proved to have certain advantages over non-selective NSAIDs and have been increasingly used for pain management in patients with OA.

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Our comprehensive analysis revealed that COX-2 inhibitors may be beneficial for suppressing aggrecan degradation and for reducing inflammatory pain by inhibiting PGE2 release, although they may have limited efficacy in suppressing collagen degradation and nerve growth. This study suggests the feedback roles of PGE2 in the negative regulation of NGF and MMP-1 and MMP-13 and the positive regulation of ADAMTS-4 and ADAMTS-5.

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One of the most striking features of inflammatory arthritis is the hyperplasia of synovial fibroblasts. It is not known whether the massive synovial hyperplasia characteristic of rheumatoid arthritis is due to the proliferation of synovial fibroblasts or to defective apoptosis. It has been found that glutamate receptor antagonists inhibit proliferation of different human tumour cells and the anticancer potential of glutamate receptor antagonists was suggested. Here, we investigated the effect of glutamate receptor antagonists and selected antirheumatic drugs on proliferation of synoviocytes in vitro. Experiments were conducted on rabbit synoviocytes cell line HIG-82 obtained from American Type Culture Collection (Menassas, VA, USA). Cell proliferation was assessed by means of 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. The IC50 value (the concentration of drug necessary to induce 50% inhibition) together with confidence limits was calculated. Glutamate receptor antagonists, 1-(4-aminophenyl)-3,5-dihydro-7,8-dimethoxy-4H-2,3-benzodiazepin-4-one (CFM-2), riluzole, memantine, 1-4-aminophenyl-methyl-7,8-methylenedioxy-5H-2,3-benzodiazepine (GYKI 52466), dizocilpine, ketamine and 2,3-dihydroxy-6-nitro-7-sulfamoylbenzo(f)quinoxaline (NBQX), inhibited proliferation of synoviocytes with the following IC50 values (in mM): 0.014, 0.017, 0.065, 0.102, 0.15, 0.435 and 1.16, respectively. Antirheumatic drugs, celecoxib, diclofenac, nimesulide, sulfasalazine, naproxen and methotrexate, inhibited proliferation of synoviocytes with the following IC50 values (in mM): 0.0043, 0.034, 0.044, 0.096, 0.385 and 1.123, respectively. Thus, the antiproliferative potential of glutamate receptor antagonists is comparable to that of antirheumatic drugs.

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Compared with recipients of nsNSAIDs, coxib recipients were less likely to switch medications and had approximately half the adjusted costs for switching-related wasted resources per prescription.

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The dynamic weight bearing (DWB) system was used for the evaluation of spontaneous behaviour changes in the zymosan-induced peritonitis mouse model. Inflammatory mediator levels were evaluated in peritoneal lavage and their correlation with the behavioural endpoints was assessed. We evaluated the effect on behavioural endpoints of the selective cyclooxygenase-2 (COX-2) inhibitor celecoxib and the Nav 1.8 blocker A-803467.

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This experiment examined and compared the effects of pre-test administration of a selective COX-2 inhibitor (celecoxib), at the doses in the range of mg/kg and ng/kg on morphine state-dependent learning in step-down passive avoidance task in mice. Pre-training administration of 5mg/kg of morphine-impaired memory retrieval tested 24h later, which was restored by pre-test administration of the same dose of the drug. Pre-test administration of celecoxib (12.5, 25 and 50mg/kg), alone or in combination with morphine (1mg/kg) prevents morphine-induced memory impairment. Ultra-low doses (ULDs) of celecoxib (2, 10 and 50 ng/kg) produced no change in morphine-induced memory impairment. However, co-administration of nanogram doses of celecoxib with 5mg/kg of morphine in the test day prevented morphine-induced memory improvement, an action different from mg/kg doses. These findings implicate the involvement of COX-2 in memory retrieval and demonstrate that the effect of celecoxib ULD is different from that of mg/kg doses.

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Abdominal aortic aneurysms (AAAs) are a chronic inflammatory disease that increase the risk of life-threatening aortic rupture. In humans, AAAs have been characterized by increased expression of cyclooxygenase-2 and the inactivation of COX-2 prior to disease initiation reduces AAA incidence in a mouse model of the disease. The current study examined the effectiveness of selective cyclooxygenase-2 (COX-2) inhibition on reducing AAA progression when administered after the initiation of AAA formation. AAAs were induced in hyperlipidemic apolipoprotein E-deficient mice by chronic angiotensin II (AngII) infusion and the effect of treatment with the COX-2 inhibitor celecoxib was examined when initiated at different stages of the disease. Celecoxib treatment that was started 1 week after initiating AngII infusion reduced AAA incidence by 61% and significantly decreased AAA severity. Mice treated with celecoxib also showed significantly reduced aortic rupture and mortality. Treatment with celecoxib that was started at a late stage of AAA development also significantly reduced AAA incidence and severity. Celecoxib treatment significantly increased smooth muscle alpha-actin expression in the abdominal aorta and did not reduce expression of markers of macrophage-dependent inflammation. These findings indicate that COX-2 inhibitor treatment initiated after formation of AngII-induced AAAs effectively reduces progression of the disease in hyperlipidemic mice.

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To assess the analgesic efficacy and adverse effects of a single oral dose of celecoxib for moderate to severe postoperative pain.

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This cyclooxygenase-1 inhibitor did not improve the strength of ligament healing but did significantly improve the strength of the contralateral uninjured ligament.

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We conclude that maternal administration of therapeutic doses of celecoxib does not adversely affect fetal renal growth. MMP-9 is increased in various nephropathies, but may also have protective effects therefore its suppression by COX-2 inhibitors needs further study.

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The rats on regular or 60% fructose-enriched diets for 6 weeks were further divided into rats combined with or without piroxicam (a selective COX1 inhibitor) or celecoxib (a selective COX2 inhibitor) treatment for an additional 2 weeks. Euglycaemic hyperinsulinaemic clamp (EHC) with a tracer dilution method was performed at the end of the study.

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The prostaglandin E2 EP1 receptor as well as the inflammatory enzyme cyclooxygenase-2 have been suggested as targets for disease modulation, improvement of therapeutic response, and restoration of pharmacosensitivity in epilepsies. Translational development of respective add-on approaches requires careful analysis of putative effects on ictogenesis. Therefore we evaluated the impact of the EP1 receptor antagonist SC-51089, the EP1 receptor agonist misoprostol and the COX-2 inhibitors celecoxib and NS-398 in the mouse amygdala kindling model of temporal lobe epilepsy. Neither celecoxib nor NS-398 affected the generation, spread and termination of seizure activity. Whereas SC-51089 did not affect the seizure threshold, the highest dose (30mg/kg) significantly decreased the seizure severity when administered 60min before stimulation. Moreover, SC-51089 significantly prolonged seizure duration at the highest dose. The EP1 receptor agonist misoprostol exerted contrasting effects on seizure duration with a significant decrease in the duration of motor seizure activity. The data suggest that doses of COX-2 inhibitors and EP1 receptor antagonists which exert disease modulating or antiepileptic drug potentiating effects do not negatively affect seizure control in temporal lobe epilepsy. The contrasting impact of the EP1 receptor antagonist and agonist suggests that EP1 receptors can influence endogenous mechanisms involved in termination of seizure activity.

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In this analysis, relative to the most frequently prescribed strength, celecoxib-treated patients with OA and RA had higher DACONs than rofecoxib-treated OA and RA patients across all subgroups. These observations may have economic implications in terms of direct effects on cost and the need for formularies to consider overall use patterns in addition to pill costs. However, these conclusions are limited by lack of clinical information (other than an OA or RA diagnosis), inability to ascertain actual use, and potential for selection bias.

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An open-label multicentre study was conducted in primary care centres in Spain to investigate the effect of a switch from celecoxib to rofecoxib among patients with osteoarthritis and to identify factors associated with a good response to rofecoxib treatment. Patients were eligible to participate in this study if their physicians considered that they might benefit from such a change of therapy. A total of 2,228 patients (1481 women) were enrolled in the study: participants' mean age was 66.37 years (SD 9.04). Mean duration of OA was 7.44 (6.38) years. Predominant sites of OA included the knee (1,132 patients, 50.8%), lumbar spine (977 patients, 43.9%) and cervical spine (739 patients, 33.2%). At baseline, most patients (77%) were being prescribed celecoxib 200 mg/day; during the study most (92.5%) received rofecoxib 25 mg/day. The mean interval between switch to rofecoxib and follow-up interview was 33 days.

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Both loxoprofen sodium and celecoxib were well tolerated for the relief of acute postoperative pain after spinal surgery. A single administration of loxoprofen showed superior and rapid effectiveness compared with celecoxib for both slight and severe postoperative pain.

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Combination treatment with ginger-partitioned acupoint stimulation at zusanli (ST 36), oral sanhuangwuji powder, and ARDs had a better clinical effect for RA with complicated peptic ulcer, compared with ARD treatmentalone or in combination with ginger-partitioned acupoint stimulation.

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We searched the following databases up to August 2004: MEDLINE, EMBASE, Cochrane Database of Systematic Reviews, Cochrane Controlled Trials Register, National Research Register, NHS Economic Evaluation Database, Health Technology Assessment Database. The bibliographies of retrieved papers and content experts were consulted for additional references.

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Controversy persists regarding the cardiovascular risks of treatment with selective cyclooxygenase 2 inhibitors (coxibs) and nonselective nonsteroidal antiinflammatory drugs (NSAIDs). This study was undertaken to examine, in a large group of new users of coxibs and NSAIDs, the rate of cardiovascular events, their time course, and whether baseline cardiovascular risk modified the rate ratios (RRs) for future events.

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Appropriate pain management affects outcome after hip fracture surgery. Although multimodal pain management is commonly used for pain control for patients undergoing elective surgery, few studies have evaluated its use in those undergoing hip fracture surgery. This prospective randomized study was designed to determine the clinical value of multimodal pain management with preemptive pain medication and intraoperative periarticular multimodal drug injections in patients undergoing bipolar hip hemiarthroplasty.

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Apocynin, Mito-TEMPO, and Celecoxib treatments prevented Ang II-induced hypertension, the increased vasoconstrictor responses to phenylephrine, and the reduced acetylcholine relaxation. The NOX-2 inhibitor gp91ds-tat, the NOX-1 inhibitor ML171, catalase, and the COX-2 inhibitor NS398 abolished the ex vivo effect of Ang II-enhancing phenylephrine responses. Antioxidant treatments diminished the increased vascular COX-2 expression, prostanoid production, and/or participation of COX-derived contractile prostanoids and thromboxane A(2) receptor (TP) in phenylephrine responses, observed in arteries from hypertensive models. The treatment with the COX-2 inhibitor normalized the increased ROS production (O(2)·(-) and H(2)O(2)), NAD(P)H Oxidase expression (NOX-1, NOX-4, and p22phox) and activity, MnSOD expression, and the participation of ROS in vascular responses in both hypertensive models. Apocynin and Mito-TEMPO also normalized these parameters of oxidative stress. Apocynin, Mito-TEMPO, and Celecoxib improved the diminished nitric oxide (NO) production and the modulation by NO of phenylephrine responses in the Ang II model.

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The overview included 39 separate Cochrane Reviews with 41 analyses of single dose oral analgesics tested in acute postoperative pain models, with results from about 50,000 participants in approximately 460 individual studies. The individual reviews included only high-quality trials of standardised design, methods, and efficacy outcome reporting. No statistical comparison was undertaken.Reliable results (high quality information) were obtained for 53 pairs of drug and dose in painful postsurgical conditions; these included various fixed dose combinations, and fast acting formulations of some analgesics. NNTs varied from about 1.5 to 20 for at least 50% maximum pain relief over four to six hours compared with placebo. The proportion of participants achieving this level of benefit varied from about 30% to over 70%, and the time to remedication varied from two hours (placebo) to over 20 hours. Good (low) NNTs were obtained with ibuprofen 200 mg plus paracetamol (acetaminophen) 500 mg (NNT compared with placebo 1.6; 95% confidence interval 1.5 to 1.8), ibuprofen fast acting 200 mg (2.1; 1.9 to 2.3); ibuprofen 200 mg plus caffeine 100 mg (2.1; 1.9 to 3.1), diclofenac potassium 50 mg (2.1; 1.9 to 2.5), and etoricoxib 120 mg (1.8; 1.7 to 2.0). For comparison, ibuprofen acid 400 mg had an NNT of 2.5 (2.4 to 2.6). Not all participants had good pain relief and, for many pairs of drug and dose, 50% or more did not achieve at least 50% maximum pain relief over four to six hours.Long duration of action (eight hours or greater) was found for etoricoxib 120 mg, diflunisal 500 mg, paracetamol 650 mg plus oxycodone 10 mg, naproxen 500/550 mg, celecoxib 400 mg, and ibuprofen 400 mg plus paracetamol 1000 mg.There was no evidence of analgesic effect for aceclofenac 150 mg, aspirin 500 mg, and oxycodone 5 mg (low quality evidence). No trial data were available in reviews of acemetacin, meloxicam, nabumetone, nefopam, sulindac, tenoxicam, and tiaprofenic acid. Inadequate amounts of data were available for nine drugs and doses, and data potentially susceptible to publication bias for 13 drugs and doses (very low quality evidence).

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Celecoxib (up to 25 microM) did not cause significant cytotoxicity in ARPE-19 or RF6A cells. Nanomolar concentrations of celecoxib reduced VEGF mRNA and VEGF protein secretion. Celecoxib-PLGA microparticles (diameter: 1140 +/- 15 nm), containing 14.93% +/- 0.21% of celecoxib sustained in vitro drug release and in vivo drug levels in the retina for 60 days. Diabetes elevated PGE2 secretion, VEGF protein, the vitreous-plasma protein ratio, and blood-retinal barrier leakage by 3-, 1.7-, 3.1-, and 2.7-fold, and celecoxib-PLGA microparticles significantly reduced these elevations by 40%, 50%, 40%, and 50%, respectively. Neither the placebo-treated eyes nor the contralateral eyes in celecoxib-PLGA microparticle-treated rats showed significant effects. Celecoxib-PLGA or placebo-PLGA particles had no effect on the body weight or blood sugar level of rats. The celecoxib-PLGA microparticles did not cause any changes in blood cell counts or chemistry and caused no histopathological damage to the retina or periocular tissues.

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Experiments were performed using bronchial carcinoma cells A549, transformed fibroblasts HH4dd, the FaDu head-and-neck tumor cells, the colon carcinoma cells HCT116, and normal fibroblasts HSF7. Effects of celecoxib treatment were assessed by clonogenic cell survival, Western analysis, and quantification of residual DNA damage by gammaH(2)AX foci assay.

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BxPC-3, MIAPaCa-2, PANC-1 and AsPC-1 pancreatic adenocarcinoma cells were exposed to sorafenib and celecoxib combined treatment in vitro. Cell viability and various growth promoting and survival signaling pathways were monitored by MTT, flow cytometry and Western blotting.

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Both nonsteroidal anti-inflammatory drugs (NSAIDs) and cyclooxygenase (COX) 2-selective inhibitors such as celecoxib are being reported as having potent anticancer activity in laboratory models. Several reports have suggested that the mechanism of action of these agents in reducing tumor volume/burden is unrelated to their inhibition of prostaglandin synthesis. Many in vitro reports use supraphysiological concentrations of these drugs to demonstrate COX-independent activities on apoptosis or proliferation. In vivo, most murine tumor models express COX-2 only in the vasculature and stroma, unlike human tumors that also express COX-2 in the tumor cells. In general, these models have the limitation of having no measurable, COX-2-derived, prostaglandins, the inhibition of which correlates with antitumor efficacy. We report here that 1483 human head and neck xenograft tumors express COX-2 similar to the pattern observed in human solid tumors and that COX-2 activity produces high levels of prostaglandin E2 (PGE2). Inhibition of COX-2 by celecoxib resulted in loss of intratumor PGE2 levels and reduced tumor growth in a dose-dependent manner. In contrast, a selective COX-1 inhibitor, SC-560, did not measurably reduce tumor prostaglandin levels or tumor growth despite the presence of COX-1 in the host and tumor cells. Celecoxib-treated tumors showed reduced proliferation and increased apoptosis of both tumor and stromal cells compared with vehicle controls. Specific inhibition of PGE2 activity by a neutralizing antibody mimicked the reduced tumor growth observed after celecoxib treatment, suggesting growth is PGE2 mediated. These data indicate that a major antitumor mechanism of action of celecoxib is inhibition of COX-2-derived prostaglandins, particularly PGE2, and suggest celecoxib as a novel therapeutic agent for human head and neck cancer.

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In all, 21 studies met the selection criteria. Across the safety analysis populations of the included studies, 7797 patients received celecoxib total daily dose 200 mg/day, 6653 received celecoxib total daily dose 400 mg/day, 2953 received naproxen, 499 received ibuprofen, and 5643 received diclofenac. Tolerability-related GI AEs were reported by significantly fewer celecoxib-treated patients (16.0%) than by those treated with naproxen (24.3%), ibuprofen (24.2%), or diclofenac (19.9%) (p < 0.0001 vs. each comparator). Time to study discontinuation due to any GI AE was significantly longer for celecoxib than for naproxen (p < 0.0001), ibuprofen (p = 0.002), or diclofenac (p = 0.048). In the RA subpopulation (n = 2857), there was no significant difference between the celecoxib and naproxen or ibuprofen groups in incidence of tolerability-related GI AEs and GI AEs.

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Celecoxib inhibits meningioma growth in vivo at plasma levels achievable in humans. Celecoxib-treated tumors were less vascular with increased apoptosis. IOMM-Lee tumors treated with celecoxib showed decreased COX-2 and VEGF expression. COX-2 inhibitors may have a role in the treatment of recurrent meningiomas.

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celebrex high dosage 2016-11-15

Nonsteroidal anti-inflammatory drugs (NSAIDs) reduce pain and inflammation by inhibiting the synthesis of prostanoids. However, these drugs inhibit both cyclooxygenase-1 (COX-1), which is essential for the regulation of homeostasis in many tissues, as well as COX-2, which is an important mediator of pain and inflammation. Disruption of COX-1 enzymatic activity by NSAIDs leads to such side effects as interference with platelet functions and gastric ulcers. The recent development of COX-2-specific inhibitors, such as celecoxib, raises the possibility of relieving pain and inflammation with reduced risk of gastrointestinal complications. In Phase II and III studies, celecoxib has demonstrated efficacy in alleviating dental pain and the signs and symptoms of osteoarthritis and rheumatoid arthritis. This COX-2-specific inhibitor was also associated with a markedly lower rate of gastroduodenal injury than is seen typically with NSAIDs. Incidence of buy celebrex most adverse events (including gastrointestinal) and withdrawal rates resulting from adverse events with celecoxib were similar to placebo. Celecoxib appears to be both safe and effective in the treatment of osteoarthritis and rheumatoid arthritis. Its COX-2-specific inhibitory properties thus introduce the possibility of effective relief of arthritic and other types of pain and inflammation with less risk of the mechanism-based toxicities observed with conventional NSAIDs.

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Cyclooxygenase-2 is a valid target for cancer prevention and treatment. This has been shown in preclinical and clinical cancer prevention studies by using a cyclooxygenase-2 inhibitor, celecoxib. When used in a randomized cancer prevention clinical trial on patients with the inherited autosomal dominant condition, familial adenomatous polyposis, celecoxib proved efficacious. However, a remarkable heterogeneity in patients' responses to the chemopreventive effects of celecoxib was observed. Proteomic profiling of sera from these patients identified several markers, the expression of which was specifically modulated after treatment with celecoxib. A decision tree algorithm identified classifiers for response to celecoxib with relatively high sensitivity but moderate to low specificity. In particular, a spectral feature at m/z 16,961.4 was identified as a strong discriminator between response and nonresponse to celecoxib at buy celebrex the highest dose.

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Direct-to-consumer advertising (DTCA) of prescription drugs is illegal in Canada as a health protection measure, but is permitted in the United States. However, in 2000, Canadian policy was changed to allow 'reminder' advertising of prescription drugs. This is a form buy celebrex of advertising that states the brand name without health claims. 'Reminder' advertising is prohibited in the US for drugs that have 'black box' warnings of serious risks. This study examines spending on DTCA in Canada from 1995 to 2006, 12 years spanning this policy shift. We ask how annual per capita spending compares to that in the US, and whether drugs with Canadian or US regulatory safety warnings are advertised to the Canadian public in reminder advertising.

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This study described for the first buy celebrex time the use of DWB as a non-subjective and non-reflexive method for the evaluation of inflammatory-driven abdominal pain in a mouse model.

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The outcome of advanced colorectal cancer (CRC) has steadily improved with the addition of several novel agents. However, chemotherapy is associated with significant toxicities such as diarrhea and bone marrow suppression. Celecoxib has been associated with decreased gastrointestinal toxicity and improved chemotherapy tolerance in preclinical in vivo models, resulting in its investigation in CRC clinical trials. These trials failed to show any improvements in efficacy or reduction in chemotherapy-induced toxicity. This article summarizes relevant preclinical and clinical investigations of celecoxib in CRC. buy celebrex

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To compare the efficacy of celecoxib for buy celebrex treatment of withdrawal headache vs prednisone in patients with medication overuse headache (MOH).

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We have demonstrated a DNA-PKcs-dependent differential modulation of cellular radiosensitivity by celecoxib. These effects might be attributed to alterations in signaling cascades downstream of DNA-PK toward cell survival. These findings offer an explanation for the poor outcomes in buy celebrex some recently published clinical trials.

celebrex cost 2015-08-10

This study was aimed at examining the buy celebrex mechanisms underlying the chemopreventive effect of celecoxib against prostate cancer. We focused our attention on events at the cellular level to show the ability of celecoxib to inhibit prostate cancer growth, by inducing cell cycle arrest and apoptosis. Moreover, we attempted to demonstrate the expression of genes involved in the downstream events related to cyclooxygenase-2 (COX-2) regulation and apoptosis.

celebrex reviews 2015 2016-03-31

Since December 2014, 14 magnetic resonance-guided focused ultrasound (MRgFUS) treatments for desmoid tumors were performed at our institution in seven patients. Nine of these treatments were completed in three patients with large tumors within the posterior thigh. The first was a 7-year-old boy who had previously been treated with surgical resection, intra-operative radiation, along with courses of vinblastine/methotrexate and sorafenib. Pretreatment tumor volume was 770 cm(3) with 75% non-enhancing volume following the buy celebrex initial treatment. The first treatment was complicated by a third-degree far-field skin burn. Enhanced safety measures were developed to protect the far-field skin. The patient had four subsequent treatments over 14 months, without complication, with non-perfused volume of 85% on current imaging. The second patient was a 21-year-old woman who had previously taken sulindac and celecoxib but had no other therapy. Pretreatment tumor volume was 740 cm(3). The lateral decubitus position was used to minimize the amount of energy through the sciatic nerve. The first treatment resulted in a relatively low non-perfused volume of 30%. A follow-up treatment resulted in 75-80% ablation of the target. The third patient was a 14-year-old girl with no prior treatment. Pretreatment tumor volume was approximately 440 cm(3). The sciatic nerve was encased by the anteromedial portion of the mass. A lateral decubitus position and enhanced safety measures were again used. The first treatment resulted in a relatively low non-perfused volume of 30%, likely related to low energies. The second treatment resulted in 70-80% ablation.

celebrex 75 mg 2017-07-27

We evaluated the effects of aggregating medications or diagnoses on hd-PS performance in an empirical example using resampled cohorts with small sample size, rare outcome incidence, or low exposure prevalence. In a cohort study comparing the risk of upper gastrointestinal complications in celecoxib or traditional NSAIDs (diclofenac, ibuprofen) initiators with rheumatoid arthritis and osteoarthritis, we (1) aggregated medications and International Classification of Diseases-9 (ICD-9) diagnoses into hierarchies of the Anatomical Therapeutic Chemical classification (ATC) and the Clinical Classification Software (CCS), respectively, and (2) sampled the full cohort using techniques validated by simulations to create 9,600 samples to compare 16 aggregation scenarios across 50% and buy celebrex 20% samples with varying outcome incidence and exposure prevalence. We applied hd-PS to estimate relative risks (RR) using 5 dimensions, predefined confounders, ≤ 500 hd-PS covariates, and propensity score deciles. For each scenario, we calculated: (1) the geometric mean RR; (2) the difference between the scenario mean ln(RR) and the ln(RR) from published randomized controlled trials (RCT); and (3) the proportional difference in the degree of estimated confounding between that scenario and the base scenario (no aggregation).

celebrex 200mg reviews 2016-08-23

Pancreatic cancer has a poor prognosis and is often diagnosed at an advanced stage, which makes it difficult to treat. The low buy celebrex survival rate of patients with pancreatic cancer points towards an increased need for novel therapeutic and chemopreventive strategies and also early detection of this disease. Increased consumption of fruits and vegetables has been associated with a reduced risk of pancreatic cancer. Synthetic and natural, diet-derived bioactive compounds have been evaluated as pancreatic cancer chemopreventive agents and have demonstrated various degrees of efficacy in cellular and in vivo animal models. Some chemopreventive agents (for example, curcumin or resveratrol) have also been reported to sensitize pancreatic cancer cells to standard chemotherapeutic drugs (for example, gemcitabine or erlotinib), which suggests that chemopreventive agents could potentially be used as potentiators of standard chemotherapy. Few clinical trials of pancreatic cancer chemopreventive agents have been completed and some are in early phases. Further development of pancreatic cancer chemopreventive agents may prove to be tremendously valuable for individuals at high risk of developing pancreatic cancer and patients who present with premalignant lesions. This Review discusses the current state of the pancreatic cancer chemoprevention field and highlights the challenges ahead.

celebrex generic 2016-05-04

We retrospectively reviewed the records of 195 patients with suspected cutaneous reactions from NSAIDs. Two hundred and six different non-steroidal anti-inflammatory drugs (NSAIDs) were suspected of causing cutaneous reactions, and the most frequent suspected causative NSAID was ibuprofen (25.7%). Angioedema and/or urticaria were the most frequent cutaneous reactions (54.4%), and the foremost suspected causative drug for these reactions was ibuprofen. The second most frequently found cutaneous reaction was buy celebrex maculopapular eruption (26.2%), and celecoxib was the most commonly suspected causative NSAID for it. The primary suspected NSAIDs causing fixed drug eruption were in enolic acid group. Furthermore, drug hypersensitivity syndrome was diagnosed in five patients, and Stevens-Johnson syndrome and toxic epidermal necrolysis were detected in five patients.

celebrex medicine 2015-09-20

Pharmaceuticals mostly exist in crystalline form and exhibit the phenomenon of differential crystal packing and configurational arrangements of molecules, called polymorphism. Pharmaceutical processing by introducing significant amount of stress alters the molecular interactions in the system engendering polymorphic transformations. The energy supplied by these processing steps tends to overcome the energy barriers between different solid-state forms, thus yielding undesirable changes in the physicochemical and material characteristics of drugs or their dosage forms. Therefore, the role of these unit processes in solid-state transformations must be cautiously studied and buy celebrex if required appropriate controls should be used to monitor such events. The present study was aimed at studying the effect of major energy imparting pharmaceutical unit processes, like size reduction, wet granulation, consolidation, and compression on solid-state transformation of Celecoxib, a selective cyclooxygenase-II inhibitor and its N,N-dimethyl acetamide and N,N-dimethyl formamide solvated forms. A qualitative estimation of crystal transformation in processed samples was performed using DSC, microscopy, FTIR spectroscopy, and XRPD. FTIR was also applied for the development of a quantification method to find the percentage of transformation in N,N-dimethyl acetamide solvated form during compression.

celebrex highest dosage 2015-10-06

The germinal matrix of premature infants is selectively vulnerable to hemorrhage within the first 48 h of life. To assess the role of vascular immaturity in buy celebrex germinal matrix hemorrhage (GMH), we evaluated germinal matrix angiogenesis in human fetuses and premature infants, as well as in premature rabbit pups, and noted active vessel remodeling in all three. Vascular endothelial growth factor (VEGF), angiopoietin-2 and endothelial cell proliferation were present at consistently higher levels in the germinal matrix relative to the white matter anlagen and cortical mantle. On that basis, we asked whether prenatal treatment with either of two angiogenic inhibitors, the COX-2 inhibitor celecoxib, or the VEGFR2 inhibitor ZD6474, could suppress the incidence of GMH in premature rabbit pups. Celecoxib treatment decreased angiopoietin-2 and VEGF levels as well as germinal matrix endothelial proliferation. Furthermore, treatment with celecoxib or ZD6474 substantially decreased the incidence of GMH. Thus, by suppressing germinal matrix angiogenesis, prenatal celecoxib or ZD6474 treatment may be able to reduce both the incidence and severity of GMH in susceptible premature infants.

celebrex generic availability 2017-05-01

Celecoxib is a potent nonsteroid anti-inflammatory drug (NSAID) that has demonstrated great promise in cancer chemoprevention and treatment. The goal of this study was to Augmentin Adult Dose determine the inhibitory effect and mechanism of celecoxib on Lewis lung carcinoma. The effect of celecoxib on viability of Lewis lung carcinoma cells was assessed with methyl thiazolyl tetrazolium (MTT) assay. Apoptosis and the mitochondrial membrane potential were detected by flow cytometric assay. The protein expression of cytosolic phospholipase A(2) (cPLA(2)), cyclooxygenase-2 (COX-2), and peroxisome proliferator-activated receptor gamma (PPARγ) were determined by Western blot analysis. The concentrations of arachidonic acid (AA) and prostaglandin E(2) (PGE(2)) in culture supernatants were measured by the methods of RP-HPLC and PGE(2)-specific ELISA, respectively. Celecoxib inhibited the proliferation of Lewis lung carcinoma and induced apoptosis in a dose-dependent manner by breakdown of mitochondrial membrane potential. The protein expressions of cPLA(2) and PPARγ were upregulated, but COX-2 protein expression was downregulated in the Lewis lung carcinoma cells exposed to celecoxib. The amount of AA was increased and PGE(2) was decreased in the culture supernatant, respectively. The ratio of AA to PGE(2) was increased in a dose-dependent manner. The major findings in this study are that celecoxib could inhibit the viability of Lewis lung carcinoma cells by interference of the AA pathway and upregulation of PPARγ simultaneously, which are novel and important since the molecular mechanisms of celecoxib underlying the anti-neoplastic effects remain unclear.

celebrex generic equivalent 2016-09-28

To clarify the role of cyclooxygenase-2 (COX-2) in acute recovery of trabecular bone in reloaded hindlimbs of tail-suspended mice, we administered a COX-2 selective inhibitor in the mice during the reloading period after unloading. Experiments were conducted on 140 male C57BL/6J mice (8 weeks old). They were divided into ground control (GC) and unloading by tail suspension (UL) groups. On day 7, Group GC was divided into Groups GC+Vehicle (Veh) and GC+Celecoxib (Cel), while Group UL mice were fed on the ground [reloading (RL)] after 7-day unloading and were then divided into Groups RL+Veh and RL+Cel. Bone histomorphometry, osteogenic cell development, and mRNA expression of osteogenic molecules were assessed. At 5 days after reloading, the increase of bone formation rate and the ratio of osteocalcin mRNA expression per CFU-f colony in Group RL+Cel were significantly decreased compared with those in Group RL+Veh, while alkaline phosphatase-positive (ALP+) CFU-f formation and the ratios of cbfa-1, osterix, and type 1 collagen mRNA expression per CFU-f colony increased to the Luvox Mg same levels in both RL groups. At 14 days after reloading, decreased bone volume by unloading in RL+Veh recovered to the same level as that of GC+Veh, but that in RL+Cel did not recover completely. The increase of c-fos mRNA expression in bone marrow cells at 1, 24, and 48 h after reloading, osteocalcin mRNA at 6 h, and osterix mRNA at 24 h were suppressed by COX-2 inhibitor. These data indicate that the COX-2 selective inhibitor celecoxib suppresses the restoration of tibial trabecular bone formation and the acute recovery of trabecular bone. These actions are closely related to restriction of c-fos and osteocalcin mRNA expressions and osteoblast differentiation in bone marrow cells.

celebrex 600 mg 2016-11-18

Glimepiride (GLI) is prescribed for the management of type-2 diabetes where as pitavastatin (PIT) for the treatment of diabetes associated dyslipidemia. Both the drugs are metabolized by CYP2C9 and have the potential of altering the enzyme through either inhibition or induction. In this respect, we present a simple, fast and validated bioanalytical LC-MS/MS method for the simultaneous estimation of GLI and PIT from rat plasma. Waters XTerra RP HPLC column (4.6×100mm, 5μm) with mobile phase consisting of acetonitrile and 10mM ammonium acetate (pH-6.0) in the ratio 85:15 (v/v) at a flow rate of 1mL/min was used for the chromatographic separation. The negative ionization mode with MRM transitions: m/z 420.17→288.13 for PIT, m/z 489.59→350.12 for GLI and m/z 380.08→ Hyzaar Medication Information 316.31for celecoxib as internal standard (IS). A total run time of 3min and LLOQ was found to be 5ng/mL for both PIT and GLI. The method was applied to study the drug interaction between GLI and PIT in rat liver microsomes. In vivo rat pharmacokinetics study showed there was a 1.29-fold increase in AUC0-∞ and 1.2-fold decrease in the clearance of PIT in presence of GLI. No notable difference in the pharmacokinetic profile of GLI was observed upon the intravenous co-administration of PIT.

celebrex dosage medscape 2015-01-26

Selective cyclooxygenase (COX)-2 inhibitors do not adversely affect renal function in experimental cirrhosis. Propecia Pills In the current study, we investigated the molecular mechanisms underlying the effects of the selective COX-2 inhibitor, celecoxib, and assessed the influence of albumin on its actions.

celebrex 2 mg 2016-04-05

To study the effects of celecoxib on the cell proliferation and expression of vascular endothelial growth factor (VEGF) in human nasopharyngeal Zofran Odt Dose carcinoma line.

celebrex drug recall 2015-02-10

Forty-five patients were enrolled. Irinotecan 125 mg/m(2) on days 2 and 8 in combination with MMC 6 mg/m(2) on day 1 every 4 weeks is recommended for future studies; myelosuppression and diarrhea are dose-limiting. The addition of celecoxib resulted in unacceptable toxicities despite reductions on irinotecan's dose. No relevant pharmacokinetic interactions occurred between irinotecan and MMC, and mean increases in Topo-1, were observed. Sixteen of 36 patients evaluable for response-assessment had discernable anti-tumor activity, including 1 complete, 4 partial, 10 minor and 1 tumor marker response. Four Levitra Effectiveness Reviews patients had prolonged (>4 months) disease-stability (stable disease, not included in CR or PR). Patients experiencing complete and partial responses had higher increments in Topo-1 expression.

celebrex 400 mg 2017-01-08

The Academic Medical Centre, Amsterdam and the Erasmus Medical Centre, Rotterdam enrolled 83 eligible patients with unresectable pancreatic cancer in a prospective multicentre phase II study. Requip Drug Abuse Median age was 62 years, median tumour size 40 mm and the majority of the patients (85%) had pancreatic head cancers. Treatment consisted of 20×2.5 Gy radiotherapy combined with UFT 300 mg/m(2) per day, leucovorin (folinic acid) 30 mg and celecoxib 80 0mg for 28 days concomitant with radiotherapy. Four patients were lost to follow-up.

celebrex alternative medication 2015-03-30

Recent evidences suggest key roles of abnormal neurogenesis and astrogliosis in the pathogenesis of epilepsy. Alterations in the microenvironment of the stem cell, such as microglial activation and cyclooxygenase-2 induction may cause ectopic neurogenesis or astrogliosis. Here, we examined if inflammatory blockade with celecoxib, a selective cyclooxygenase-2 inhibitor, could modulate the altered microenvironment in the epileptic rat brain. Celecoxib attenuated the likelihood of developing spontaneous recurrent seizures after pilocarpine-induced prolonged seizure. During the latent period, celecoxib prevented neuronal death and microglia activation in the hilus and CA1 and inhibited the generation of ectopic granule cells in the hilus and new glia in CA1. The direct inhibition of precursor cells by celecoxib was further demonstrated in human neural stem cells culture. These findings raise the evidence of COX-2 induction to act importantly on epileptogenesis and suggest a potential therapeutic role for COX-2 inhibitors in chronic epilepsy.

celebrex 50 mg 2016-02-04

To assess analgesic efficacy and adverse effects of a single oral dose of celecoxib for moderate to severe postoperative pain.

celebrex dosing instructions 2015-07-23

We performed a randomized, controlled, crossover trial to assess the effect on INR of celecoxib versus codeine (control treatment) in 15 patients who were receiving warfarin therapy and required analgesic treatment for osteoarthritis. During Phase 1 of the study, patients were randomly allocated to receive celecoxib 200 mg/day or codeine phosphate 7-15 mg 3-4 times daily for 5 weeks. During Phase 2 of the study, patients stopped the first study medication and started the other study medication; there was no drug-free interval between phases. Weekly INR testing was performed during the 10 week study period. Adopting the intent-to-treat principle, we used generalized estimating equations to analyze the data.

celebrex normal dosage 2017-05-02

This was a retrospective case-control study based on insurance claims, with chart review to confirm cases. The base population consisted of 2.2 million adult users of celecoxib, diclofenac, ibuprofen, naproxen, rofecoxib, or valdecoxib who were covered by commercial health insurance in the United States from 1999-2003. For 790 persons hospitalized for PUBP and 7887 controls, most recent NSAID/COX-2 use and a variety of medical and pharmacy risk factors were ascertained from the insurance files and analyzed by conditional logistic regression. The main outcome measure was the odds ratio (OR) associated with use of each drug by comparison to naproxen, and in successive intervals after last dispensing.