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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:
Acicox, Aclarex, Articox, Artilog, Artose, Artrixib, Caditar, Celcox, Celcoxx, Celebra, Celeco, Celecoxibum, Celemax, Celenta, Celib, Celosti, Celox-r, Celoxib, Celoxx, Cexb, Ciox, Cloxib, Colcibra, Coxalgen, Coxbit, Coxib, Coxibrex, Coxlec, Dicoxib, Dilox, Dolocox, Dorex, Dorit, Ezy, Flaxel, Flonar, Impedil, Inibrex, Lexfin, Medocel, Onsenal, Radicacine, Revibra, Selecox, Sionara, Solexa, Thritex, Zycel

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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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COX-2 expression in human gastric cancer cell lines SGC-7901, BGC-823, MGC-803 and AGS were measured at the mRNA and protein level. COX-2 rich cell line SGC-7901 was chosen for subsequent experiments. siRNA mediated gene knockdown was used to investigate the impact of COX-2 on nuclear factor-κB (NF-κB), Snail, and E-cadherin in gastric cancer cells. Gene expression was determined by Western blot and real-time polymerase chain reaction. To analyze whether NF-κB inhibition could interrupt the modulatory effect of COX-2 or prostaglandin E2 (PGE2) on E-cadherin, gastric cancer cells were treated with celecoxib or PGE2, in the presence of NF-κB specific siRNA.

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We assessed 120 patients (83 women and 37 men) who had experienced adverse reactions to one or more NSAIDs; 64 (53.3%) of them had reacted to only one NSAID (single reactors) and 56 (46.7%) to multiple NSAIDs (multiple reactors). Among our subjects, 76.7% reported cutaneous reactions, 8.3% respiratory symptoms, 10.8% both cutaneous and respiratory symptoms, and 4.2% anaphylaxis. All patients were subjected to a single-blind, placebo-controlled oral challenge with two different doses of celecoxib (50 + 150 mg 1 h later = cumulative dose of 200 mg).

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Two compounds (celecoxib and valdecoxib) from the diarylheterocycle class of cyclooxygenase inhibitors were radiolabeled and used to characterize their binding to cyclooxygenase-1 (COX-1), cyclooxygenase-2 (COX-2), several single-point variants of COX-2 (Val523Ile, Tyr355Ala, Arg120Ala, Arg120Gln, Arg120Asn) and one triple-point variant of COX-2 [Val523Ile, Arg513His, Val434Ile (IHI)]. We demonstrate highly specific and saturable binding of these inhibitors to COX-2. Under the same assay conditions, little or no specific binding to COX-1 could be detected. The affinity of [(3)H]celecoxib for COX-2 (K(D) = 2.3 nM) was similar to the affinity of [(3)H]valdecoxib (K(D) = 3.2 nM). The binding to COX-2 seems to be both rapid and slowly reversible with association rates of 5.8 x 10(6)/M/min and 4.5 x 10(6)/M/min and dissociation rates of 14 x 10(-3)/min (t(1/2) = 50 min) and 7.0 x 10(-3)/min (t(1/2) = 98 min) for [(3)H]celecoxib and [(3)H]valdecoxib, respectively. These association rates increased (4- to 11-fold) when the charged arginine residue located at the entrance to the main hydrophobic channel was mutated to smaller uncharged amino acids (Arg120Ala, Arg120Gln, and Arg120Asn). Mutation of residues located within the active site of COX-2 that define a 'side pocket' (Tyr355Ala, Val523Ile, IHI) of the main channel had a greater effect on the dissociation rate than the association rate. These mutations, which modified the shape of and access to the 'side pocket', affected the binding affinity of [(3)H]valdecoxib more than that of [(3)H]celecoxib. These binding studies provide direct insight into the properties and binding constants of celecoxib and valdecoxib to COX-2.

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We previously reported that cycloogenase (COX)-2-generated prostaglandin E2 (PGE2) had anti-apoptotic effects in UVB-exposed mouse skin that involved EP2-mediated signaling (Chun et al., Cancer Res. 2007; 67: 2015). Because survivin is a regulator of cell survival, the possible involvement of COX-2 and EP2 in survivin expression following UVB exposure of mouse skin was investigated. In wild type mice, UVB exposure time-dependently increased the levels of survivin and phosphorylated-signal transducer and activator of transcription 3 (p-STAT3), a transcription factor that regulates survivin expression; and COX-2- or EP2-deficiency significantly reduced their induction. Topical application of the COX-2 inhibitor, celecoxib, also reduced UVB-induced survivin levels. To further investigate the roles of PGE2 and EP2 in the regulation of survivin, indomethacin was used to inhibit UVB-induced endogenous PG production. UVB-induced survivin levels were reduced by indomethacin, and PGE2 and the EP2 agonist, butaprost, partially restored survivin levels. The epidermal growth factor receptor (EGFR) is a downstream effector of EP2 and EGFR inhibition (AG1478) significantly reduced UVB activation of STAT3 and survivin levels. UVB-induced epidermal apoptosis in COX-2-/- mice was reduced by butaprost and EGFR inhibition blocked butaprost’s protective effects. Furthermore, butaprost in the absence of UVB exposure time-dependently increased p-EGFR, p-STAT3, and survivin levels in naïve mouse skin, whereas the EP4 agonist, PGE1 alcohol, did not significantly increase p-STAT3 or survivin levels. These data suggest that COX-2-generated PGE2 regulates survivin expression in mouse skin, in part, via an EP2-mediated EGFR/STAT3 pathway. Therefore, targeting the EP2/survivin pathway may provide a strategy for the chemoprevention/chemotherapy of skin cancer.

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Overexpression of cyclooxygenase-2 (COX-2) is associated with carcinogenesis, invasiveness, and metastasis of malignant tumors. Inhibition of COX-2 is one hot topic of research in prevention and treatment of malignant tumors. Because of the selective and specific inhibition on the activity of COX-2, the roles of celecoxib in prevention and treatment of tumors have attracted broad attention in recent years. In this study, we investigated the inhibitory effect of celecoxib combined with cisplatin on the proliferation of human tongue squamous cell carcinoma cell line Tca8113 in vivo and in vitro.

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Peptides designed from osteoprotegerin (OPG) have previously been shown to inhibit receptor activator of NF-κB ligand (RANKL) and prevent bone loss without significantly inhibiting inflammation. The objective of this study was to develop a novel peptide with dual inhibitory activity against bone loss and inflammation using site-directed mutagenesis. Out of the three putative sites (i.e., Tyr70-Asp78, Tyr82-Glu96, and Leu113-Arg122) available on OPG for RANKL binding, Leu113-Arg122 was used as a template for peptide synthesis. Peptide mutants of the template sequence (112YLEIEFCLKHR122) were synthesized and initially screened for their inhibitory effect on RANK-RANKL binding by competitive ELISA. The most active peptide was further evaluated in vitro for RANKL induced osteoclastogenesis in mouse macrophage cells, and in vivo for Freund's complete adjuvant induced arthritis (AIA) in Lewis rats. The efficacy of the candidate peptide was compared with that of the standard drug celecoxib. The peptide YR-11 (YLEIEFSLKHR), obtained by direct substitution of cysteine with a serine residue in the template sequence, significantly (p<0.05) inhibited RANK-RANKL binding, and RANKL induced TRAP activity and formation of multinucleated osteoclasts without any cytotoxicity. Administration of YR-11 peptide at the dose of 30mg/kg (i.p.) ameliorated both bone loss and inflammation in AIA rats. To elucidate the mechanism for inhibition of inflammation in arthritic rats, serum and tissue cytokines (TNF-α, IL-1β, and IL-6) were analyzed by ELISA and RT-PCR methods. Results confirmed that YR-11 peptide inhibited pro-inflammatory cytokines in the sera and hind paw tissues of AIA rats through its suppressive effect on RANKL induced nuclear translocation of NF-κB. The results obtained in this study substantiate the therapeutic benefit of this novel peptide in the prevention of bone loss and inflammation in rheumatoid arthritis with reduced side effects.

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Since cancer cells depend on glucose more than normal cells, we compared the effects of low carbohydrate (CHO) diets to a Western diet on the growth rate of tumors in mice. To avoid caloric restriction-induced effects, we designed the low CHO diets isocaloric with the Western diet by increasing protein rather than fat levels because of the reported tumor-promoting effects of high fat and the immune-stimulating effects of high protein. We found that both murine and human carcinomas grew slower in mice on diets containing low amylose CHO and high protein compared with a Western diet characterized by relatively high CHO and low protein. There was no weight difference between the tumor-bearing mice on the low CHO or Western diets. Additionally, the low CHO-fed mice exhibited lower blood glucose, insulin, and lactate levels. Additive antitumor effects with the low CHO diets were observed with the mTOR inhibitor CCI-779 and especially with the COX-2 inhibitor Celebrex, a potent anti-inflammatory drug. Strikingly, in a genetically engineered mouse model of HER-2/neu-induced mammary cancer, tumor penetrance in mice on a Western diet was nearly 50% by the age of 1 year whereas no tumors were detected in mice on the low CHO diet. This difference was associated with weight gains in mice on the Western diet not observed in mice on the low CHO diet. Moreover, whereas only 1 mouse on the Western diet achieved a normal life span, due to cancer-associated deaths, more than 50% of the mice on the low CHO diet reached or exceeded the normal life span. Taken together, our findings offer a compelling preclinical illustration of the ability of a low CHO diet in not only restricting weight gain but also cancer development and progression.

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The patients in the multimodal treatment group had a significantly reduced intraoperative opioid requirement, as measured by the mean morphine equivalent dose administered (38.4 ± 2.73 mg vs 49.1 ± 2.65 mg; P < .01). The mean postoperative opioid use was also significantly reduced (10.7 ± 2.82 mg vs 26.2 ± 6.56 mg; P = .034), as was the mean total morphine equivalent dose administered (49.1 ± 2.7 mg vs 75.3 ± 4.6 mg; P < .001). The operative time, estimated operative blood loss, antiemetic use, postoperative creatinine and hemoglobin levels, and length of stay were similar in the 2 groups. No operative or treatment complications occurred in either group.

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The authors searched trial registers for current Phase II clinical trials on cachexia. Twelve studies were found with 11 compounds, including the anti-inflammatory drugs thalidomide, OHR/AVR118, celecoxib, VT-122, omega-3 supplements, and anabolic agents such as ghrelin analogues, MT-102, BYM338 and ruxolotinib. The authors note that one of the studies related to COPD while the others were related to different cancers. Herein, the authors describe the mechanisms of action and their Phase II study design.

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Twenty-four patients who were undergoing long-term treatment with aspirin (100 mg daily) for cardioprotection were coadministered celecoxib, 200 mg twice daily, ibuprofen, 600 mg 3 times daily, or placebo for 7 days.

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celebrex reviews 2015-02-23

VAS scores, sleep disturbance, PCA cumulative volumes of the Zanaflex 4 Mg Tablet fentanyl were significantly better in the multimodal groups compared with the simple analgesia group (P<0.05), the opioid and celecoxib related adverse effects were not statistically lower in the multimodal groups (P>0.05). The observation group was more satisfied with analgesia treatment and experienced less pain 1 month after discharge (P<0.05).

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This method allowed comparison of Zantac 150 Generic common treatments of knee OA according to their relative efficacy. Intra-articular treatments were superior to nonsteroidal anti-inflammatory drugs, possibly because of the integrated IA placebo effect. Small but robust differences were observed between active treatments. All treatments except acetaminophen showed clinically significant improvement from baseline pain. This information, along with the safety profiles and relative costs of included treatments, will be helpful for individualized patient care decisions.

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This article presents a critical look at studies of patients with Coumadin Medicine MOHs. It appears that the withdrawal strategy remains the best treatment option, although there is scant evidence on the efficacy of any treatment options.

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Epidemiological studies have revealed a protective effect of NSAIDs, which principally target cyclooxygenase (COX)-1 and COX-2, on the development of colorectal cancer. Increased expression of COX-2 was shown in colorectal adenocarcinoma. However, some effects were shown to be Augmentin 375 Mg COX-independent. Here, we compared two selective COX-2 inhibitors for their effect on the growth of colorectal tumour cells in vitro.

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A new reversed-phase, isocratic LC method was developed for the quantitative determination of COX-2 inhibitor celecoxib in bulk drugs and in pharmaceutical dosages. The proposed method is also applicable for the purity evaluation of celecoxib in bulk drugs Accutane 80 Mg 6 Months . 5-Methyl 2-Nitro phenol has been used as internal standard for the quantitative determination of celecoxib. The method has been completely validated and proven to be rugged. The limit of detection (LOD) and limit of quantitation (LOQ) for celecoxib impurities namely, 4-hydrazino benzene sulfonamide (Intermediate I) and 1-(4-methyl phenyl)-4,4.4-trifluro butan-1,3-dione (Intermediate II) were found to be 32.0 and 97 ng. respectively. The active pharmaceutical ingredient was extracted from its finished dosage form (capsule) using methanol. The percentage recoveries ranged from 90.7 to 93.8. The stability studies were performed for celecoxib solution placed on laboratory bench and in refrigerator for hundred days. The samples were found to be stable for the study period.

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The purpose of this study was to investigate the effects of Celecoxib on the Geodon Capsules proliferation of the FLT3-ITD positive and negative acute myeloid leukemia cells and its mechanism. The proliferation inhibition effect of Celecoxib with different doses on the FLT3-ITD positive cells MV4-11 and the FLT3-ITD negative K562 cells was detected by CCK-8 method, the cell apoptosis was determined by flow cytometry, and the MEK, Mcl-1, pAKT expression was tested by Western blot. The results showed that Celecoxib inhibited the proliferation of both MV4-11 and K562 cells, but the IC50 for MV4-11 was (29.14 ± 2.4) µmol/L, which was significantly lower than that of K562 cells (39.84 ± 1.0) µmol/L (P < 0.05); The induced apoptosis rate of Celecoxib at 20-80 µmol/L on MV4-11 was not observed, but there was apparent influence on K562 at the same concentration. Western blot showed that Celecoxib down-regulated the expression of MEK and Mcl-1 but did not change the expression of pAKT obviously on MV4-11 cells, while the expression of Mcl-1 was reduced a little, but no obvious change were found in the expression of MEK and pAKT on K562 cells. It is concluded that the Celecoxib can inhibit the proliferation of FLT3-ITD positive AML cells distinctly, and the potential mechanism may be related to the inhibition of the MEK/Mcl-1 signaling pathway.

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The study enrolled 150 chronic celecoxib users and 216 non-users who underwent pan-endoscopy to detect H. pylori infection and its related intestinal metaplasia. One hundred and three H. pylori-infected patients with intestinal metaplasia (43 chronic celecoxib users and 60 non-users) received anti-H. pylori therapy and completed the 12-month follow-up to survey the regression of intestinal metaplasia Levitra With Alcohol by mean intestinal metaplasia score.

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The purpose of this study was to determine whether patients treated under this protocol were less likely to exhibit postoperative fever after Mobic 15 Mg Tablet Information primary TJA, compared with a historical control group, and whether they were less likely to receive postoperative testing as part of a fever workup.

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All experiments were conducted in human non-small-cell lung carcinoma (NSCLC) cell lines; results in celecoxib-treated Vigrx Enhancement Pills and untreated cells were compared. Cell survival was assessed with a sulforhodamine B assay. Apoptosis was assessed by DNA fragmentation with an enzyme-linked immunosorbent assay, by terminal deoxynucleotidyltransferase-mediated dUTP nick-end-labeling (TUNEL) assay, and by western blot analysis of caspase activation. Death receptor gene and protein expression was detected by northern and western blot analysis, respectively. Gene silencing was achieved with small interfering RNA (siRNA) technology.

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The selective cyclooxygenase-1 inhibitor, SC-560, will improve the strength of ligament healing in Priligy Buy Online Uk an in vivo rat model.

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The National Institute for Health and Clinical Excellence (NICE) health economic model for assessing the Requip Xl Generic Drug cost-effectiveness of celecoxib plus a proton pump inhibitor (PPI) compared to diclofenac plus PPI in the treatment of osteoarthritis has been updated using new adverse event (AE) risks from the CONDOR trial. In light of this new information, this study aimed to evaluate the incremental cost-effectiveness ratio (ICER) of celecoxib plus PPI compared to diclofenac plus PPI.