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Feldene

Feldene is a qualitative medication which is taken in treatment of pain or inflammation, which are caused by arthritis. Feldene effectiveness is in reducing hormones that cause inflammation and pain in the body. It is nonsteroidal anti-inflammatory drug (NSAIDs).

Other names for this medication:

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Also known as:  Piroxicam.

Description

Feldene is a perfect remedy in struggle against pain or inflammation caused by arthritis.

Feldene effectiveness is in reducing hormones that cause inflammation and pain in the body. It is nonsteroidal anti-inflammatory drug (NSAIDs).

Feldene is also known as Piroxicam, Dolonex.

Dosage

Take Feldene tablets orally with food.

Do not crush or chew it.

Take Feldene at the same time with water for 2 weeks.

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

Overdose

If you overdose Feldene and you don't feel good you should visit your doctor or health care provider immediately. Symptoms of Feldene overdosage: vomiting, stomach pain, feeling drowsy, coughing up blood, shallow breathing, fainting, coma, nausea, black or bloody stools.

Storage

Store below 30 degrees C (86 degrees F) away from moisture, light 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 Feldene 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.

Contraindications

Do not take Feldene if you are allergic to Feldene components.

Do not take Feldene if you are pregnant, planning to become pregnant. Avoid breast-feeding.

Be careful with Feldene if you are taking a blood thinner such as warfarin Coumadin), lithium (Eskalith, Lithobid), methotrexate (Rheumatrex, Trexall), steroids (prednisone and others), aspirin or other NSAIDs (non-steroidal anti-inflammatory drugs) such as etodolac (Lodine), flurbiprofen (Ansaid), indomethacin (Indocin), ketoprofen (Orudis), ketorolac (Toradol), mefenamic acid (Ponstel), nabumetone (Relafen), naproxen (Aleve, Naprosyn), piroxicam (Feldene), and others, or an ACE inhibitor such as benazepril (Lotensin), captopril (Capoten), fosinopril (Monopril), enalapril (Vasotec), lisinopril (Prinivil, Zestril), ramipril (Altace), diuretics (water pills) such as furosemide (Lasix), meloxicam (Mobic).

Be careful with Feldene if you suffer from stroke, blood clot, heart disease, congestive heart failure, a history of stomach ulcers or bleeding, liver or kidney disease, asthma, polyps in your nose, a bleeding or blood clotting disorder, if you smoke, from heart attack, high blood pressure.

Avoid prolonged exposure to sunlight.

Avoid alcohol.

It can be dangerous to stop Feldene taking suddenly.

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To determine the efficacy and toxicity of chemotherapy in the treatment of canine nasal tumours.

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This work studied the mechanisms of interaction between Eudragit RS100 (RS) and RL100 (RL) polymers with 3 nonsteroidal anti-inflammatory drugs: diflunisal (DIF), flurbiprofen (FLU), and piroxicam (PIR). Solid dispersions of polymers and drugs at different weight ratios were prepared by coevaporation of their ethanol solutions. The resulting coevaporates were characterized in the solid state (Fourier-transformed infrared spectroscopy (FT-IR) IR, differential scanning calorimetry, powder-x-ray diffractometry) as well as by studying the in vitro drug release in a gastroenteric environment. Absorption tests from drug solutions to the solid polymers were also performed to better explain the mechanism of interactions between them. The preparative conditions did not induce changes in the crystalline state of the drugs (amorphization or polymorphic change). Drugs strongly interacted with the ammonium groups present in polymers, giving an electrostatic interaction that reinforced the mere physical dispersion of drug molecules within polymer networks. Such interactions are related to the chemical structure of the drugs and to their dissociated or undissociated state. The dispersion of drugs in the polymer matrices strongly influenced their dissolution rate, which appeared slower and more gradual than those of the pure drugs, when polymer ratios were increased. RL coevaporates usually displayed higher dissolution rates. The kinetic evaluation of the dissolution profile, however, suggested that both the drug solubility in the external medium and its diffusion capacity within the polymer network are involved. In the sorption experiments, RL showed a greater adsorptive capacity than RS, in relation to the greater number of quaternary ammonium functions, which behave as activity sites for the electrostatic interactions. In the presence of Tris-HCl buffer (pH 7.4), drug adsorption was reduced, as a consequence of the competition of the chloride ions with drug anions for the polymer binding sites. In general, DIF and FLU displayed a similar interaction with RS and RL active sites; PIR's was different. The different molecular structures of these agents can justify such findings. The presence of a carboxyl group (instead of another dissociable acidic moiety, like the hydroxy-enolic one in the PIR molecule) could help explain the strong interaction with RS and RL polymers' quaternary ammonium centers. Preliminary studies like ours are important in helping develop better forecasting and increasing the understanding of the incorporation/release behavior of drugs from particulate delivery systems that can be made from these polymers.

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We hypothesized that continuous treatment with low-dose cyclophosphamide and full-dose piroxicam would delay tumor recurrence in dogs with soft tissue sarcomas (STS).

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The 23 criterion-meeting studies included a total of 92,532 participants, with mixed results. Sulindac was the only specific agent to have been studied with formal audiometry in a randomized double-blind placebo-controlled trial in which hearing was the reported primary outcome: Although an effect was seen in the unadjusted analysis (pure tone threshold>15 dB, 9.3% vs 2.9%; relative risk [RR], 3.2; confidence interval [CI], 1.09-9.55; P=.02), the effect dissipated in the adjusted analysis (P=.09). There was a significant effect on self-reported hearing loss from NSAIDs as a class (RR, 1.21; CI, 1.11-1.33), ibuprofen (RR, 1.13; CI, 1.06-1.19), and acetaminophen (RR, 1.21; CI, 1.11-1.33), but no formal audiometric data confirm or refute this suggested effect. Audiometry has demonstrated profound loss in some instances of acetaminophen-narcotic combination ingestions.

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This work was undertaken to assess the protective effect of an isoflavonoid, calycosin-7-O-beta-D-glucopyranoside (CG), isolated from Astragali radix (AR) on the pathogenesis of osteoarthritis (OA)-like lesion in a rabbit model.

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An interactive in vitro cultivation system composed of human chondrocyte alginate cultures and conditioned supernatant of SV40 T-antigen immortalised human synovial fibroblasts was used. Chondrocyte alginate cultures were stimulated with supernatant of RA synovial fibroblasts, of healthy donor synovial fibroblasts, and of RA synovial fibroblasts that have been antirheumatically treated with disease-modifying antirheumatic drugs (DMARDs) (azathioprine, gold sodium thiomalate, chloroquine phosphate, and methotrexate), nonsteroidal anti-inflammatory drugs (NSAIDs) (piroxicam and diclofenac), or steroidal anti-inflammatory drugs (SAIDs) (methylprednisolone and prednisolone). Chondrocyte gene expression profile was analysed using microarrays. Real-time reverse transcription-polymerase chain reaction and enzyme-linked immunosorbent assay were performed for validation of microarray data.

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The free radical reactivity of a number of currently prescribed non-steroidal anti-inflammatory drugs (NSAIDs) (sulindac, diflunisal, piroxicam, naproxen, ibuprofen, indomethacin and aspirin) was studied by observing their action on the free radical polymerization of acrylamide initiated by the thermal decomposition of potassium peroxodisulfate in aqueous solution at pH 7 and 50°C. Analysis of the kinetics of the polymerization reaction showed that sulindac, diflunisal, piroxicam, indomethacin and aspirin reacted directly with the carbon-centred polyacrylamide free radicals, thereby retarding the polymerization. The specific rate constants for reaction of sulindac, diflunisal, piroxicam, indomethacin and aspirin with polyacrylamide radicals at pH 7, ionic strength 0.1 M and 50°C were found to be 6850, 262, 76, 30 and 21 M(-1) s(-1) respectively. The reaction mechanism is postulated to involve reduction of the drug. On the other hand, naproxen and ibuprofen were able to react with the initiating SO4(•-) radicals, causing inhibition of the polymerization and oxidation of the drug. This study verifies the ability of NSAIDs to react as free radical scavengers and potentially to participate as a chain breaking agent in 'oxidative stress' in biological systems. Among them, sulindac is the most selective and effective when interacting with the carbon-centred radicals, and this may be a reflection of the rapid reduction in vivo of sulindac to its active sulphide metabolite.

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There were marked differences in the permeation kinetics of ranitidine, metoprolol, and piroxicam. The possibility of an association between absorption kinetics from dosage forms in humans and Caco-2 monolayer permeability may allow for a direct kinetic interpretation of human oral absorption from Caco-2 monolayer permeability values.

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In order to improve prescription practice and the profile of drug usage in the population, it is important to educate health care professionals, and to inform general population about the risks of inappropriate drug use.

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The effect of piroxicam in three different formulations was tested on rabbits for 28 days in an alkali burn model. The ulceration healing process was determined by evaluating the severity of the burn (scored from 0 to 5), and the re-epithelization healing process was measured by the area of the defects. The results indicated that the piroxicam positively charged submicron emulsion was the most effective formulation in lowering the ulcerative cornea score while the piroxicam positively charged emulsion and the blank emulsion were more effective in promoting the re-epithelization healing process. The piroxicam solution elicited the slowest healing re-epithelization rate after 28 days and was unable to complete the entire healing process. The new positively charged submicron emulsion formulation of piroxicam had a pronounced effect on both the ulceration rate and epithelial defects in the management of corneal alkali-burning.

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Patients in group 1 reported significantly lower pain scores (P < 0.05) at all time intervals except at 24 hours and better global assessment (P = 0.001) than did group 2. There were significantly fewer patients in the preemptive group than group 2 who required rescue analgesic within the first 24 hours (0% vs 22.7%; P = 0.024). Mean time to first analgesic request was also significantly longer in the preemptive group (P = 0.001).

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Shockwave lithotripsy (SWL) is one of the most important treatment modalities for urinary stone disease. The procedure may cause pain, and patient relaxation and cooperation are crucial in maintaining stone localization for optimal fragmentation and patient comfort during the procedure. As yet, there is not a standard analgesic protocol for patients undergoing SWL. We aimed to use three different analgesic agents and compare their efficacy during SWL in this study.

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Drug distribution within the microspheres was examined using confocal fluorescence microscopy. The rate of polymer degradation was determined as the change in molecular weight, measured by gel permeation chromatography, during in vitro degradation experiments. Further, changes in the surface and interior morphology of the particles during in vitro degradation were investigated by scanning electron microscopy.

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The nitrogen- and sulfur-containing 1,2-benzothiazines meloxicam and piroxicam are widely used as nonsteroidal anti-inflammatory drugs. Intrigued by the presence of multiple donor atoms and therefore potentially rich coordination chemistry, we prepared a series of organometallic Ru and Os compounds with meloxicam and piroxicam featuring either as mono- or bidentate ligand systems. The choice of the solvent and the pH value was identified as the critical parameter to achieve selectively mono- or bidentate coordination. The coordination modes were confirmed experimentally by NMR spectroscopy and single crystal X-ray diffraction analysis. Using DFT calculations, it was established that complexes in which meloxicam acts as a bidentate N,O donor are energetically more favorable than coordination as O,O and S,O donor systems. Since meloxicam and piroxicam derivatives have shown anticancer activity in the past, we aimed to compare the complexes with mono- and bidentate ligands on their in vitro anticancer activity. However, stability studies revealed that only the latter complexes were stable in [D6 ]DMSO/D2 O (5:95) and therefore no direct comparisons could be made. The meloxicam complexes 1 and 2 showed moderate cytotoxicity, whereas the piroxicam derivatives 5 and 6 were hardly active against the utilized cell lines.

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A double-blind multicentre study was conducted to compare the efficacy and safety of tenoxicam and ketoprofen in the treatment of osteoarthritis (OA). The study comprised 307 patients and the treatment period was 12 weeks. One-hundred and fifty-five patients received 20 mg tenoxicam once-daily and 152 patients received 100 mg ketoprofen b.i.d. Seventy-seven patients were prematurely withdrawn; 32 patients in the tenoxicam group and 45 in the ketoprofen group (p less than 0.05). There were only small insignificant differences in the efficacy parameters with the exception that significantly more patients in the tenoxicam group took paracetamol tablets during treatment. Adverse events developed in 29.0% of the patients on tenoxicam and in 47.3% of the patients on ketoprofen, this difference was statistically significant (p less than 0.05). The adverse events were predominantly from the gastrointestinal tract and the central nervous system. No serious side-effects occurred and the laboratory parameters showed no clinically relevant changes. The investigator's overall impression of treatment showed no significant difference between groups. Excellent or good results were judged in 55.2% of the patients on tenoxicam and in 62.1% on ketoprofen (p greater than 0.05). Tenoxicam appears to have a reasonable balance between efficacy and side-effects in the treatment of OA.

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Conclusively, melt sonocrystallization offered an efficient, solvent-free technique that can be exploited for particle designing of drugs with favorable pharmaceutical properties.

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A total of 334 patients received standard therapy (n = 246) or standard therapy plus lornoxicam (n = 88), 172 (51.5%) of whom developed systemic complications. Occurrence of complications was higher with standard therapy compared with lornoxicam (57.3% versus 35.2%; P = 0.00034), as was mortality (19.1% versus 6.8%; P = 0.006). The TLR2 and TLR4 expression and TLR2 and TLR4-mediated cytokine production were significantly higher in patients with systemic complications of acute pancreatitis compared with healthy volunteers. Relative TLR2 expression and cytokine production were significantly reduced in patients receiving lornoxicam versus standard therapy.

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To enhance analgesia, the combinatorial use of analgesic drugs with proven efficacies is a widely-used strategy to reduce adverse side effects. The present study characterizes the antinociceptive interaction of intrathecal morphine co-administered with different NSAIDs using isobolographic analysis.Antinoceptive activity was evaluated using a model for acute visceral pain, the writhing test of mice. The possible involvement of opioid receptors in the mechanism of action of the intrathecal co-administration of morphine and NSAIDs was investigated using the non-selective receptor antagonist naltrexone. The study demonstrated a synergistic antinociception of intrathecal administered combinations of morphine with the following NSAIDs: diclofenac, ketoprofen, meloxicam, metamizol, naproxen, nimesulide, parecoxib and piroxicam. The supra additive effect was obtained with very low doses of each drug and it appeared to be independent of the COX-1 or COX-2 inhibition selectivity of each NSAID and was not significantly modified by intrathecal naltrexone. The findings of the present work suggest that the combination of opioids and NSAIDs has a direct action on spinal nociceptive processing, which may be achieved via mechanisms that are independent of the activation of opioid receptors. The ineffectiveness of naltrexone to reverse the analgesic activity of opioids + NSAIDs combinations indicates that other complex pain regulatory systems are involved in this effect.

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Inflammation may increase cancer risk, therefore, we studied whether polyphenol-rich Marie Ménard (MM) apples with reported anti-inflammatory activity prevent 1,2-dimethylhydrazine (DMH)-induced colon carcinogenesis in rats and, likewise whether high-fat (HF) diet promoting carcinogenesis, may affect inflammation. DMH-induced rats were fed for 15 weeks with: an HF diet (23% corn oil w/w); an HF diet containing 7.6% w/w lyophilized MM (apple diet (AD)); a low-fat (LF) diet and an HF diet containing piroxicam (PXC) (0.01% w/w) as control. Mucin depleted foci (MDF), precancerous lesions in the colon, were dramatically reduced in the AD, LF, and PXC groups compared with the HF. Peritoneal macrophage activation, an index of systemic inflammation, was significantly decreased in the AD, LF, and PXC groups. TNF-α, iNOS, IL-1β, IL-6 m-RNA expression in the colon, as well as CD68 cells and plasmatic PGE2 were lower in the AD, but not in the LF group. Apoptosis in the MDF of both the AD and LF-fed rats was significantly higher than in HF rats. In conclusion, AD has a strong chemopreventive effect, reducing inflammation, and increasing apoptosis, while the chemopreventive effect of the LF diet seems mediated mainly by increased apoptosis in MDF.

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Few analytical techniques allow to evaluate the inclusion yield of cyclodextrin-drug complexes, because most manufacturing processes give amorphous products. In this study, we have developed an alternative method to differential scanning calorimetry, to accurately determine the free/complexed piroxicam ratio by UV spectroscopy. This method is based on the differential solubility of the piroxicam-beta-cyclodextrin 1:2.5 mol/mol complex in water-acetonitrile (1:1, v/v) (Solvent A) or in anhydrous acetonitrile (Solvent B), both containing 0.05 M HCl. In anhydrous acetonitrile, beta-cyclodextrin is insoluble and the included drug remains entrapped, allowing the free piroxicam determination, while with 50% of water, the complex is totally dissolved, allowing the determination of the total guest content. This method was validated for linearity, precision and accuracy. The presence of cyclodextrin does not influence the assays, but more than 0.5% of water in Solvent B significantly affects the determination of the free piroxicam content. In comparison with differential scanning calorimetry, both detectability and precision were improved. It is now possible to analyse complexes with an inclusion purity greater than 99%.

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Tomography and magnetic resonance imaging localized activated cathepsins to the inflamed colon of piroxicam-treated il10(-/-) mice. Confocal imaging detected activated cathepsins in colonic macrophages and spinal neurons and microglial cells of mice with colitis. Gel electrophoresis and immunoprecipitation identified activated Cat-B, Cat-L, and Cat-S in colon and spinal cord, and Cat-S was preferentially secreted into the colonic lumen. Intraluminal Cat-S amplified visceromotor responses to colorectal distension and induced hyperexcitability of colonic nociceptors, which required expression of protease-activated receptor-2. Cat-S deletion attenuated colonic inflammatory pain induced with trinitrobenzene sulfonic acid.

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Two hundred ninety-eight patients with post-operative pain after the surgical removal of an impacted third molar were randomly assigned, on a double-blind basis, to receive a single oral dose of piroxicam 20 mg, or piroxicam-beta-cyclodextrin equivalent to 20 mg piroxicam, or paracetamol 500 mg, or placebo. Using a semi-quantitative self-rating scale, patients rated their pain and its relief at 30-min intervals for the first 2 h, and then hourly for 4 h after treatment administration. All active medications were reported to be significantly superior to placebo. The three active drugs were comparable for the degree of analgesia up to the third hour, after which the effect of paracetamol decreased significantly as compared to piroxicam-beta-cyclodextrin and piroxicam. Piroxicam-beta-cyclodextrin and paracetamol were more rapid than piroxicam in inducing analgesia. The tolerability for the active drugs was comparable to that for placebo.

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To determine whether the use of a nonsteroidal antiinflammatory drug (NSAID) in patients with painful osteoarthritis (OA) of the knee would result in alterations in specific biomechanical parameters of gait.

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The efficacy of piroxicam 20 mg/qd was compared with that of sulindac 200 mg twice a day in 49 patients with rheumatoid arthritis. Both nonsteroidal anti-inflammatory agents showed statistically significant improvement in efficacy variables including duration of morning stiffness, disease activity as judged by the examiner and by the patient, patient assessment of feeling, total joint pain, total joint swelling, and performance of daily activities. The overall frequency of adverse reactions was similar with both treatment regimens, and required discontinuance in three patients in each treatment group. However, the number of moderate/severe adverse reactions in the sulindac-treated patients was greater than that in the piroxicam-treated patients, and there was a trend toward the differences between the two groups being statistically significant (P = .06). Both drugs were effective in the treatment of rheumatoid arthritis and resulted in comparable improvement in efficacy variables.

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Patients with osteoarthritis (OA), a condition characterized by cartilage degradation, are often treated with steroids, nonsteroidal anti-inflammatory drugs (NSAIDs), and cyclooxygenase-2 (COX-2) selective NSAIDs. Due to their inhibition of the inflammatory cascade, the drugs affect the balance of matrix metalloproteinases (MMPs) and inflammatory cytokines, resulting in preservation of extracellular matrix (ECM). To compare the effects of these treatments on chondrocyte metabolism, TNF-α was incubated with cultured chondrocytes to mimic a proinflammatory environment with increasing production of MMP-1 and prostaglandin E2 (PGE2). The chondrocytes were then treated with either a steroid (prednisone), a nonspecific COX inhibitor NSAID (piroxicam), or a COX-2 selective NSAID (celecoxib). Both prednisone and celecoxib decreased MMP-1 and PGE-2 production while the nonspecific piroxicam decreased only the latter. Both prednisone and celecoxib decreased gene expression of MMP-1 and increased expression of aggrecan. Increased gene expression of type II collagen was also noted with celecoxib. The nonspecific piroxicam did not show these effects. The efficacy of celecoxib in vivo was investigated using a posttraumatic OA (PTOA) mouse model. In vivo, celecoxib increases aggrecan synthesis and suppresses MMP-1. In conclusion, this study demonstrates that celecoxib and steroids exert similar effects on MMP-1 and PGE2 production in vitro and that celecoxib may demonstrate beneficial effects on anabolic metabolism in vivo.

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Non-steroidal anti-inflammatories (NSAIDs) are analgesic, antipyretic, and, as their name implies, anti-inflammatory drugs, which are widely used for the treatment of a variety of human and veterinary disease conditions in which control of pain and inflammation is desired. Acetaminophen (ACE) is a common over-the-counter analgesic. Detection of a variety of widely used NSAIDs and ACE in fluid and tissue samples is an important diagnostic tool. A sensitive and selective analytical method has been developed for simultaneous screening of 12 NSAIDs and ACE by liquid chromatography-mass spectrometry with an atmospheric pressure chemical ionization interface set to operate in the negative ion mode of MS. Following sample preparation, all analytes were separated on a C18-reversed-phase column with a gradient elution of acetonitrile and acetic acid. Full-scan mass spectral fragmentation profiles were established for each analyte and individual extracted ion chromatograms were used for quantitation. Linearity of detection was observed over the 0.05-25.0 microg/mL range of standard concentrations. The instrument limits of detection (LOD), based on an individual analyte quantitation ions, fell between 0.05 and 1.0 microg/mL for all compounds. The matrix LODs were determined to be 0.05 microg/mL for phenylbutazone (m/z 307); 0.1 microg/mL for indomethacin (m/z 312), flunixin (m/z 295), and piroxicam (m/z 330); 0.5 microg/mL for ACE (m/z 150), diclofenac (m/z 250), ketoprofen (m/z 209), and mefenamic acid (m/z 240); 1.0 microg/mL for oxyphenbutazone (m/z 323); 5.0 microg/mL for ibuprofen (m/z 205), salicylic acid (m/z 137), and tolmetin (m/z 212); and 10 microg/mL for naproxen (m/z 185).

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feldene gel buy 2015-08-05

Form I and form II of lornoxicam were prepared by recrystallization and characterized by X-ray powder diffractometry (XRPD), thermal analysis, Fourier transform infrared feldene buy spectroscopy and scanning electron microscopy. The solubility and dissolution of both polymorphs were also determined and compared to provide the basis for polymorph selection in formulation.

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The current study investigates the effect of a post processing treatment on feldene buy dissolution performance of SD in comparison to their performances upon production.

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Three cases of skin reactions that occurred in patients under oral administration of Piroxicam are reported here: one erythema-multiforme-like reaction and two cases of acute, pruriginous erythemato-papulous dermatitis, one of which with intraepidermal blister formation. No past history of skin disease could be formed; lesions spontaneously improved when the drug was stopped. Only in one patient, receiving Piroxicam and Fenoprofene, an acute nephritis was observed. The role Flagyl Drug Study of Piroxicam, a new non-steroid antiinflammatory agent in the pathogenesis of the skin reactions observed is discussed. However, the renal involvement formed in one case is likely due to Fenoprofene, as in previously reported cases.

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The effects of intracerebroventricular (i.c.v.) administration of calcitonin and PGE2 on intestinal motility and body temperature were examined in conscious rats chronically fitted with intraparietal electrodes in the small intestine, a cannula in a cerebral lateral ventricle and a subcutaneous thermistor probe. Both calcitonin and PGE2 restored the fasted pattern of intestinal motility in fed rats and induced an increase in body temperature. Indomethacin, an inhibitor of the cyclooxygenase with calcium antagonistic properties, and TMB-8, an intracellular calcium antagonist, blocked the effects of calcitonin on intestinal motility and body temperature. Piroxicam, an inhibitor of Cymbalta 70 Mg the cyclooxygenase which does not affect calcium uptake blocked the thermic but not the intestinal effects of calcitonin. TMB-8 but not indomethacin or piroxicam partially blocked the effects of PGE2 on both intestinal motility and body temperature. It is concluded that the central hyperthermic effect of calcitonin is mediated through the formation and the release of prostaglandins whereas the central action of calcitonin on digestive motility results from intracerebral effects on calcium fluxes.

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Administration of DSS for 7 days resulted in severe acute colitis that was associated with a marked increase in stool and colon tissue TNF levels. Initiation of therapy with intraperitoneal (i.p.) LMP-420 on day 4 of DSS exposure decreased colonic TNF to near normal levels on day 7. However, neither i.p. nor oral treatment with LMP-420 affected the development or severity of acute DSS colitis. Initiation of LMP-420 therapy after 3 cycles of DSS administration to establish chronic colitis Mestinon 60mg Tablets also had no effect on the severity of chronic colitis. Analysis of colonic TNF combined with longitudinal analysis of TNF and TNF receptor (TNF-RII) levels in stool during the development of chronic DSS colitis demonstrated that the initially elevated colonic TNF levels returned to normal despite intense on-going inflammation in mice with chronic colitis. RAG-2-/- mice deficient in T and B cells also developed severe ongoing colitis in response to 3 cycles of DSS, but showed marked differences vs. wild type mice in stool TNF and TNF-RII in response to DSS exposure. Systemic and oral LMP-420 treatment for 16 days decreased colonic TNF levels in IL-10-deficient mice with chronic colitis, with a trend to decreased histologic inflammation for oral LMP-420.

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An exhaustive systematic search was performed. Inclusion criteria were: RCT or controlled study, duration of 5 days at least, inactive control, assessment of minor or major Imitrex Drug Classification NSAID adverse effects, publication range January 1985 to January 2003. The publications retrieved were assessed during a specifically dedicated WHO meeting including leading experts in all related fields. Statistics were performed conservatively. Meta-regression was performed by regressing NSAID adjusted estimates against study duration categories.

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1. Rabbit small intestinal segments containing Peyer's patches (PP) were examined in Ussing chambers using short-circuit current (Isc) recording. By comparison with control small intestinal mucosal segments, rabbit PP-containing epithelia exhibited decreased basal Isc, increased transepithelial resistance (TER) and unchanged potential difference (PD). 2. Carbachol caused a decrease in Isc in rabbit PP epithelia. Forskolin, dibutyryl cyclic GMP, histamine and the calcium ionophore, A23187, were without effect. In contrast, control epithelial segments of rabbit intestine responded to carbachol and forskolin with an increased Isc, indicative of electrogenic chloride secretion. The EC50 for carbachol was approximately 2 microM in both types of epithelia. Methacholine also caused an outward current in rabbit PP epithelia which had similar properties to that of carbachol. The effect of the cholinomimetics on rabbit PP was basolateral-sided, reversible, and sensitive to low concentrations of the general muscarinic cholinoceptor blockers, atropine, scopolamine and also to the M1 cholinoceptor blocker, pirenzepine. 3. The Isc response to cholinomimetics in rabbit PP was insensitive to bumetanide, amiloride, TEA, barium, acetazolamide, piroxicam and omeprazole, but was attenuated in the presence of ouabain. Using bilaterally-substituted solutions, the carbachol effect on rabbit PP Isc was abolished in chloride/bicarbonate-free, but not in chloride-free solutions Lasix 40 Mg , suggestive of stimulation of electrogenic bicarbonate absorption by the agent. Substitution for sodium abolished both the basal current and the Isc response to carbachol. Part of the effect of carbachol on PP Isc appeared to be mediated by submucosal neurones because addition of tetrodotoxin reduced the effect by 60%. 4 As microfold (M) epithelial cells predominate in the PP of the rabbit, the unusual phenotype of cholinomimetic-induced outward current may be used as an electrophysiological marker for these potential sites of oral vaccine delivery, and in particular it may also be of use as a marker for rabbit M cells.

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The effect of piroxicam on neutrophil and monocyte chemotaxis was evaluated in vitro and in vivo. Piroxicam demonstrated a marked inhibitory activity on neutrophil chemotaxis and to a lesser extent on monocyte chemotaxis. The data here presented supports the notion that piroxicam interfere with the inflammatory process by affecting primarily neutrophil and to a lesser degree monocyte function. Priligy Uk Reviews

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Eighty male Sprague-Dawley rats underwent surgical transection of their medial collateral ligament. Postoperatively, 20 rats were given SC-560 at a low dose and 20 at a high dose for the first 6 days of recovery; the other 40 Diflucan Online received a normal diet. The animals were sacrificed 14 days later, and both the injured and uninjured ligaments were mechanically tested to failure in tension.

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The present results suggest that the selective COX-2 inhibitor etoricoxib could be a better option than non-selective COX inhibitors, since it presented a potent inhibitory effect on the clinical signals and also a potent inhibition on Antabuse 500 Mg cell migration.

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The three currently available once-a-day treatments for osteoarthritis were compared in a double blind crossover trial. 90 patients received benoxaprofen 600 mg daily, slow-release indomethacin (Indocid-R) 75 mg daily and piroxicam 20 mg daily for three weeks each. The three compounds were comparable in efficacy. Benoxaprofen caused more side effects than the other two drugs and slow-release indomethacin caused slightly more than piroxicam. Despite the greater incidence of side effects, a number of patients still preferred benoxaprofen and elected to continue taking it. Individual preference remains the most important factor in choosing an anti-inflammatory drug for osteoarthritis.

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The interactions between piroxicam (Px) and hydroxypropyl-beta-cyclodextrin (HPbetaCD) were thoroughly investigated both in solution and the solid state. The solubility studies have demonstrated the formation of a Px:HPbetaCD inclusion complex with 1:1 stoichiometry. The addition of propylene glycol to the medium produced less stable complexes, revealing the fact of this co-solvent probably acting as a competing agent. Equimolecular Px:HPbetaCD solid systems were prepared using the co-precipitation method and then fully characterized by X-ray diffractometry, infrared spectra and differential scanning calorimetry. A topical gel formulation containing Px, as inclusion complex with HPbetaCD, was developed in order to study the influence of Px complexation on its release rate and skin percutaneous permeation. The formation of Px:HPbetaCD complexes did not increase either Px release from the vehicle or its skin permeation. However, Px complexation with HPbetaCD allowed the incorporation of a higher quantity of Px into the gel, which resulted in a considerable increase in the Px released and permeated. Skin pretreatment with different HPbetaCD solutions, followed by the application of control gel, showed no enhancing capacity. The amount of Px retained in the skin, after pretreatment experiments, was found to be very similar to that obtained without skin pretreatment and was observed to be related to flux values through the skin.

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The effects of combined single oral treatments with non-steroidal anti-inflammatory drugs (NSAIDs) and the non-competitive N-methyl-D-aspartate (NMDA) receptor antagonist dextromethorphan (DM) on arthritic pain were examined in a rat model of adjuvant-induced arthritis. Although 12.5-100 mg/kg doses of DM alone produced no reliable effects, treatments with ibuprofen (IB, 50 and 100 mg/kg but not 12.5 or 25 mg/kg) produced mild analgesia in arthritic rats as determined using the Randall-Sellito test. IB showed a dose-response relationship which appeared to plateau at doses of 50 and 100 mg/kg. Adding 50 mg/kg DM to each IB dose resulted in significantly greater analgesic activity than IB alone at doses of 25, 50 and 100 mg/kg. A similar interaction between 50 mg/kg DM and 50 mg/kg IB occurred with respect to spontaneous pain behavior. Adding 25 mg/kg DM to 25 mg/kg IB likewise increased analgesia as measured by both the Randall-Sellito and spontaneous pain behavior tests (both P < 0.05). Five more NSAIDs were evaluated using the Randall-Sellito test, which included naproxen (NP), piroxicam (PIR), etodolac (ET), diclofenac (DC), and ketorolac (KE). For all six NSAIDS, the addition of 50 mg/kg DM reliably increased their analgesic potency, as indicated by reliable increases in previously effective NSAID doses (all six NSAIDs) as well as previously ineffective NSAID doses (IB, NP, DC, and PIR). These data demonstrate that DM greatly potentiates the analgesic activity of IB, DC, NP, PIR, ET, and KT and increases the peak effect over the NSAIDs alone. Similiar to DM's previously demonstrated enhancement of opioid analgesia in acute pain, the combination of DM and an NSAID may represent a novel analgesic approach to improved management of arthritic pain.

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Two sensitive and rapid flow-injection spectrophotometric methods are proposed for the determination of tenoxicam (TX). In the first method, a Fe(III)-tenoxicam complex is formed in a methanolic medium and the absorbance is measured at 540 nm, while the second method involves measurement of the absorbance at 355 nm of a solution containing the drug in hydrochloric acid medium. In both methods, the peak heights were proportional to tenoxicam concentration over the ranges 7.0-320 and 0.5-8.5 mg/l(-1), respectively. The methods have been applied to the routine determination of the drug in dosage forms.

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Our previous studies have shown that dietary piroxicam, a non-steroidal anti-inflammatory drug (NSAID), and D,L-alpha-difluoromethylornithine (DFMO), an ornithine decarboxylase (ODC) inhibitor, act as potential chemopreventive agents in inhibiting azoxymethane (AOM)-induced colon carcinogenesis in male F344 rats. The present study was designed to determine the effect of these chemopreventive agents on intermediate biomarkers, namely colonic epithelial cell proliferation and levels of prostaglandins, which can be used as effective predictors of colon cancer. Starting at 6 weeks of age, groups of animals were fed the control diet and experimental diets containing piroxicam or DFMO. At 7 weeks of age, all animals, except the vehicle controls, were injected s.c. with AOM at a dose level of 15 mg/kg body wt/week for 4 weeks. Vehicle controls received an equal volume of normal saline. Groups of animals were then killed at the end of last AOM or saline injection (baseline) and at week 4, 16, 24 and 32 following the last AOM or saline treatment. Animals intended for cell proliferation study were injected with bromodeoxyuridine (BrdU) at a dose level of 20 mg/kg body wt 1 h prior to being killed. The rate of colonic cell proliferation at all time points was assessed immunohistochemically using anti-BrdU. The levels of colonic mucosal prostaglandins were estimated by radioimmunoassay. The results indicate that carcinogen treatment increased the colonic cell proliferation measured as the crypt labeling index in proximal and distal colons and the concentrations of colonic prostaglandin E2 (PGE2) and 6-keto PGF1 alpha. The data demonstrate that DFMO significantly inhibited the AOM-induced labeling index in the distal and proximal colon at all time points, whereas piroxicam slightly decreased the labeling index. On the other hand, piroxicam exerted a pronounced inhibitory effect on the levels of both PGE2 and 6-keto PGF1 alpha. DFMO suppressed the colonic PGE2 levels to a lesser degree than piroxicam. The results demonstrate that DFMO, an inhibitor of ODC, suppresses cell proliferation, whereas piroxicam, a NSAID, inhibits prostaglandins, and emphasize the need to develop agent-dependent intermediate biomarker(s) to validate the efficacy of chemopreventive agent(s) in colon carcinogenesis.

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Six hundred forty-four patients and 1268 controls were recruited. The odds ratio for upper gastrointestinal complications in users compared with nonusers of NANSAIDs increased with age: < or = 59 years, odds ratio 2.0; 60-79 years, odds ratio 3.0; > or = 80 years, odds ratio 4.2; and was higher in women (5.4) than in men (1.9). There was a linear dose-response curve that was steeper in women than in men. Combined exposure suggested additive risks: NANSAIDs and aspirin, odds ratio 6.7; NANSAIDs and alcohol, odds ratio 6.0 NANSAIDs by the oral route were associated with an odds ratio of 2.3, compared with 11.4 with rectal administration. Piroxicam was associated with the highest risk, odds ratio 4.8; and ibuprofen the lowest risk, odds ratio 0.7.

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The practical working conditions were established. In the 0.2 divided by 2.0 microg/mL range of piroxicam concentration, were used the 2 mL of ferric ferricyanide 1 mL of 2N hydrocloric acid. To delay the flocculation of Prussian Blue it was to add a 1 mL solution of sodium lauryl sulfate 1%. After 15 minutes read the absorbance at 760 nm. The developed method was validated.

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Non-steroidal anti-inflammatory drugs (NSAIDs) with cyclooxygenase (COX) inhibitory activity are commonly used in various inflammatory diseases. In this study, to examine the immunomodulatory effects of well known NSAIDs at clinically available doses, macrophage- and T cell-mediated immune responses such as tumor necrosis factor (TNF)-alpha release and nitric oxide (NO) production, cell-cell adhesion, phagocytic uptake and lymphocyte proliferation were investigated. NSAIDs tested significantly enhanced TNF-alpha release from lipopolysaccharide (LPS)-activated RAW264.7 cells at certain concentrations (fenoprofen, indomethacin, piroxicam, aceclofenac, diclofenac and sulindac) or in a dose-dependent manner (aspirin and phenylbutazone). Of NSAIDs, phenylbutazone and aspirin most potently attenuated NO production, although sulindac was the only compound with cytoprotective activity against LPS-induced cytotoxicity. Most NSAIDs used displayed weak or no modulatory effects on phagocytic uptake and CD29- or CD43-mediated cell-cell adhesion. Interestingly, however, phenylbutazone itself triggered cell-cell clustering under normal culture conditions and enhanced the phagocytic activity. Aspirin and phenylbutazone also dose-dependently attenuated CD4+ T cell proliferation stimulated by concanavalin A (Con A) and CD8+ CTLL-2 cell proliferation induced by interleukin (IL)-2. Sulindac only blocked CTLL-2 cell proliferation. These results suggest that NSAIDs may differentially exert immunomodulatory effects on activated macrophages and lymphocytes, and some of the effects may enforce NSAID's therapeutic effect against inflammatory symptoms.

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Preoperative administration of 80 mg methylprednisolone achieves better control of trismus than tenoxicam without any significant differences in edema and pain control in impacted third molar teeth extraction.

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Two groups, each composed of 20 elderly patients suffering from osteoarthritis characterised by intense pain, were treated for 4 weeks with the oral formulation of two modern oxicam derivatives (tenoxicam capsules and beta-cyclodextrin-piroxicam tablets respectively). The analysis of the results showed that both drugs have an excellent antalgic effect. After the first dose the action of beta-cyclodextrin-piroxican was quicker and more marked, with statistically significant differences between treatments for the first 4 hours. At the end of the study period the two drugs proved to be equally effective, with a more pronounced symptomatic effect of beta-cyclodextrin-piroxican. No side effects serious enough to warrant suspension of treatment were observed: the only side effects reported were gastric adverse events (pyrosis, gastralgia) in both groups, having an incidence of 50% (tenoxicam) and 15% (beta-cyclodextrin-piroxicam) respectively.

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A 54-year-old woman took an overdose of 1 800 mg piroxicam. She complained of nausea and abdominal pain. Endoscopy revealed multiple superficial ulcerations in the pyloric antrum and the first part of duodenum. There were no symptoms or signs from other organ system and recovery was uneventful. The highest serum concentration was 241.6 mg/l, which is about 30 times the usual therapeutic level of 5-10 mg/l.

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Multiple cytochrome P450 isoforms (P450 1A2, 2C8 and 2C9) appear to be involved in naproxen demethylation, although 2C9 appears to be the predominant form.

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Nested case-control study.

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For compounds undergoing passive intestinal absorption permeabilities were generally higher in co-cultures than in Caco-2 monolayers, yielding highest values in pure HT29-MTX monolayers. This difference was most obvious for compounds transported via the paracellular pathway, where HT29-MTX cells may be up to 30 times more permeable than Caco-2 cells, whereas for lipophilic and highly permeable compounds, the difference in permeability values was less obvious. For drugs undergoing intestinal secretion mediated by P-glycoprotein, co-cultivation of Caco-2 cells with HT29-MTX cells led to increased apical to basolateral permeability which was decreased in the opposite direction, consistent with the fact that HT29-MTX cells do not express P-glycoprotein. When a carrier-mediated absorption mechanism is involved, the permeabilities observed were lower than the values reported for human small intestine and co-cultivation of HT29-MTX cells with Caco-2 cells resulted in even lower values as compared to the plain Caco-2 cultures.

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Certain nonsteroidal anti-inflammatory drugs antagonize the action of antihypertensive therapy. Indomethacin has been shown to abrogate the antihypertensive effect of beta-adrenergic receptor blockers, diuretics, converting enzyme inhibitors, and several antihypertensive drug combinations, and the accumulated evidence on piroxicam indicates that it also raises arterial pressure in treated patients. In contrast, sulindac and aspirin do not reverse the effects of antihypertensive drugs, and currently available data indicate that they are the safest cyclooxygenase inhibitors for use in hypertensive patients. In the absence of definitive information on the array of other nonsteroidal anti-inflammatory drugs, they should be considered to pose a risk similar to indomethacin until proved otherwise. The magnitude of the elevation in blood pressure varies between patients, ranging from no effect to dangerous hypertensive responses. Generalized inhibition of the cyclooxygenase enzyme has opposing effects on arterial pressure, lowering renin on one hand and causing sodium retention on the other. Some evidence suggests that cyclooxygenase inhibition causes the greater increments in pressure in patients who initially have low plasma renin activity (often the elderly). The potential for cerebral vascular catastrophes attends these drug interactions in which platelet function also is suppressed by cyclooxygenase inhibition.

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The total synovial fluid volume (P<0.05) was most strikingly reduced by the treatment with CG. Moreover, the CG treatment also significantly alleviated the OA-induced accumulation of prostaglandin (PG) (P<0.001) and total proteins (P<0.001) in the synovial fluid. The histopathologic analyses revealed that the CG treatment reduced the severity of the OA-like structural damages in the cartilage. However, the level of PGE(2), a pathologic inflammatory molecule, was not diminished by CG or piroxicam.

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Comparative assessment of analgesics, by employing 2 PCA apparatuses in one patient, allows evaluation of the efficacy of analgesics added to the conventional methods.

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The effect of 9 nonsteroidal anti-inflammatory drugs on the renal excretion of uric acid was studied in patients with normal renal function. Diflunisal, Azapropazone and Indomethacin caused an increase and Piroxicam a decrease in the uric acid excretion. Other drugs studied had no significant influence.

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Reactive oxygen radicals are probably involved in the pathogenesis of human and experimental models of renal disease, yet current methods are inadequate to quantify and identify the cells producing reactive oxygen radicals.

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The NSAID piroxicam (PRX) drug was used for complex formation reactions with Cu(II), Zn(II) and Pt(II) metal salts have been synthesized. Then, these complexes have been characterized by spectroscopic and analytical techniques. Thermal behavior of the complexes were also investigated. The electrochemical properties of all complexes have been investigated by cyclic voltammetry (CV) using glassy carbon electrode. The biological activity of the complexes has been evaluated by examining their ability to bind to fish sperm double strand DNA (FSFSdsDNA) with UV spectroscopy. UV studies of the interaction of the PRX and its complexes with FSdsDNA have shown that these compounds can bind to FSdsDNA. The binding constants of the compounds with FSdsDNA have also been calculated. The morphology of the FSdsDNA, PRX, metal ions and metal complexes has been investigated by scanning electron microscopy (SEM). To get the SEM images, the interaction of compounds with FSdsDNA has been studied by means of differential pulse voltammetry (DPV) at FSdsDNA modified pencil graphite electrode (PGE). The decrease in intensity of the guanine oxidation signals has been used as an indicator for the interaction mechanism. The effect of proliferation PRX and complexes were examined on the HeLA and C6 cells using real-time cell analyzer with four different concentrations.

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The oral analgesic activities (ED50's) of 15 NSAIDs were determined in the phenylquinone-induced writhing test in mice. ED50 values (mg/kg) were: acetylsalicylic acid (182), fenclofenac (168), phenylbutazone (129), ibuprofen (82.2), diflunisal (55.6), benoxaprofen (25.4), naproxen (24.1), mefenamic acid (20.7), indomethacin (19.0), meclofenamate sodium (9.60), sulindac (7.20), fenoprofen calcium (3.70), tolmetin (1.30), zomepirac sodium (0.70), and piroxicam (0.44). Significant linear correlations were found between mouse ED50 values and the various recommended human analgesic or anti-inflammatory dosages. Thus, analgesic ED50 values (mg/kg p.o.) in mice (X) may be used to predict human dosages (Y) of NSAIDs according to the equation Y = 8.26X + 535, where Y is the projected human daily dosage (mg).