The world's first wiki where authorship really matters (Nature Genetics, 2008). Due credit and reputation for authors. Imagine a global collaborative knowledge base for original thoughts. Search thousands of articles and collaborate with scientists around the globe.

wikigene or wiki gene protein drug chemical gene disease author authorship tracking collaborative publishing evolutionary knowledge reputation system wiki2.0 global collaboration genes proteins drugs chemicals diseases compound
Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
Chemical Compound Review

Meloxivet     (8E)-8-[hydroxy-[(5-methyl- 1,3-thiazol-2...

Welcome! If you are familiar with the subject of this article, you can contribute to this open access knowledge base by deleting incorrect information, restructuring or completely rewriting any text. Read more.

Disease relevance of Mobic

  • We describe a patient who presented with bloody diarrhoea after 15 mg meloxicam daily for 10 days for osteoarthritis [1].
  • Ischaemic colitis in a patient taking meloxicam [1].
  • Patients were randomly allocated to receive therapy with meloxicam oral suspension, 0.125 mg/kg body weight in a single daily dose; meloxicam oral suspension, 0.25 mg/kg body weight in a single daily dose; or naproxen, 10 mg/kg body weight in 2 daily doses [2].
  • In turn, PGE(2) bolus resulted in a partial recovery of functional hyperemia, with the CBF response recovering to 52 +/- 3% and the BOLD response to 56 +/- 2% of their values prior to MEL administration [3].
  • BACKGROUND: Although clinical trial results suggest that meloxicam has less gastrointestinal toxicity than most other non-steroidal anti-inflammatory drugs (NSAIDs), in practice it has been associated with a large number of yellow card reports of gastrointestinal complications [4].

Psychiatry related information on Mobic

  • Behavioral changes including locomotor activity, passive avoidance, and spatial learning and memory ability were examined two weeks after the last administration of meloxicam [5].

High impact information on Mobic

  • The safety of cyclo-oxygenase 2 (COX-2) preferential inhibitors such as meloxicam is debated [1].
  • HGF/SF accelerated the angiogenic process in the murine implant, and this activity was inhibited by COX-2-selective meloxicam and NS398 [6].
  • Apart from this, structurally different COX inhibitors (indomethacin, meloxicam, NS-398) mediated significant inhibition of time-dependent and EGF-induced mdr1b mRNA overexpression, resulting in enhanced intracellular accumulation of the mdr1 substrate, rhodamine 123 (Rho123) [7].
  • COX inhibitors, including coxibs, nonselective nonsteroidal antiinflammatory drugs (NSAIDs), and meloxicam, were prescribed to a larger proportion of osteoarthritis patients (68.4%) than rheumatoid arthritis patients (47.1%) in our study (P < 0.001) [8].
  • Response rates according to the ACR pediatric 30 criteria improved from month 3 to month 12, as follows: from 63% to 77% in the meloxicam 0.125 mg/kg group, from 58% to 76% in the meloxicam 0.25 mg/kg group, and from 64% to 74% in the naproxen group [2].

Chemical compound and disease context of Mobic


Biological context of Mobic

  • PATIENTS: Using the UK General Practice Research Database, this study included 7.1 thousand patient years (tpy) exposure to meloxicam, 1.6 tpy exposure to coxibs, and 628 tpy exposure to older non-specific NSAIDs [4].
  • Clinical pharmacokinetics of meloxicam. A cyclo-oxygenase-2 preferential nonsteroidal anti-inflammatory drug [14].
  • Only high concentrations of meloxicam caused apoptosis and upregulated Bax mRNA and protein in MG-63 cell culture [15].
  • CONCLUSION: On the basis of free synovial concentrations and the IC50 for stimulated COX activity, meloxicam is expected to have a long duration of action [16].
  • Meloxicam is eliminated after biotransformation to 4 pharmacologically inactive metabolites, which are excreted in urine and faeces [14].

Anatomical context of Mobic

  • OBJECTIVE: To explore the effect of the nonsteroidal antiinflammatory drugs (NSAIDs) piroxicam and meloxicam on quantitative and qualitative changes in leukocyte adhesion receptors induced by cytokines and other activation stimuli [17].
  • METHODS: After a single oral dose of meloxicam 15mg, synovial fluid and blood samples were collected once per patient at various intervals after administration [16].
  • The effects of meloxicam (a COX-2 inhibitor) on the growth of two colon cancer cell lines that express COX-2 (HCA-7 and Moser-S) and a COX-2 negative cell line (HCT-116) were evaluated [18].
  • OBJECTIVE: To investigate the distribution of meloxicam in the human knee joint and to compare it with the inhibition of cyclo-oxygenase (COX) activity in synovial cells [16].
  • To investigate whether meloxicam exerted a direct effect on the cachectic process, studies on protein degradation were carried out using C(2)C(12) mouse myoblasts in response to a proteolysis-inducing factor (PIF) [19].

Associations of Mobic with other chemical compounds


Gene context of Mobic

  • Two selective COX-2 inhibitors, meloxicam and NS398, decreased HIF-1alpha levels and nuclear localization, under both normoxic and hypoxic conditions [24].
  • METHODS: COX-1 inhibition was determined by measuring thromboxane B2 (TXB2)-generation from clotting whole blood ex vivo after single oral doses of 7.5 and 15 mg meloxicam and 75 mg diclofenac and at steady state (15 mg meloxicam daily and 150 mg diclofenac daily) [21].
  • Meloxicam: selective COX-2 inhibition in clinical practice [25].
  • The in vivo findings confirm the results of in vitro tests, conducted separately, showing that meloxicam preferentially inhibits COX-2 over COX-1 [26].
  • These results suggest that PGE(2) may be produced mainly via COX-2 in this model and that meloxicam may inhibit COX-2 in the inflammatory site [27].

Analytical, diagnostic and therapeutic context of Mobic

  • Both MEL and PGE(2) had a significant effect on the activation-elicited CBF (P < 10(-6)) and BOLD (P < 10(-6)) responses, without affecting the baseline perfusion [3].
  • METHODS: We pooled data from clinical trials of meloxicam at doses of 7.5 or 15 mg/d. A blinded gastrointestinal adjudication committee used prespecified criteria to identify gastric or duodenal perforation, gastric outlet obstruction, or hemodynamically important upper gastrointestinal bleeding [28].
  • Randomized clinical trials comparing the frequency of GI adverse events for meloxicam versus non-COX-2-selective NSAIDs were selected [29].
  • Meloxicam concentrations were determined by a validated high performance liquid chromatography assay, protein binding by equilibrium dialysis, and pharmacokinetic parameters were calculated by noncompartmental analysis from the mean drug concentration-time profiles [16].
  • Meloxicam (5), an NSAID in the enol-carboxamide class, was developed on the basis of its antiinflammatory activity and relative safety in animal models [30].


  1. Ischaemic colitis in a patient taking meloxicam. Garcia, B., Ramaholimihaso, F., Diebold, M.D., Cadiot, G., Thiéfin, G. Lancet (2001) [Pubmed]
  2. A randomized, double-blind clinical trial of two doses of meloxicam compared with naproxen in children with juvenile idiopathic arthritis: short- and long-term efficacy and safety results. Ruperto, N., Nikishina, I., Pachanov, E.D., Shachbazian, Y., Prieur, A.M., Mouy, R., Joos, R., Zulian, F., Schwarz, R., Artamonova, V., Emminger, W., Bandeira, M., Buoncompagni, A., Foeldvari, I., Falcini, F., Baildam, E., Kone-Paut, I., Alessio, M., Gerloni, V., Lenhardt, A., Martini, A., Hanft, G., Sigmund, R., Simianer, S. Arthritis Rheum. (2005) [Pubmed]
  3. Modulatory role of cyclooxygenase-2 in cerebrovascular coupling. Stefanovic, B., Bosetti, F., Silva, A.C. Neuroimage (2006) [Pubmed]
  4. Channelling bias and the incidence of gastrointestinal haemorrhage in users of meloxicam, coxibs, and older, non-specific non-steroidal anti-inflammatory drugs. MacDonald, T.M., Morant, S.V., Goldstein, J.L., Burke, T.A., Pettitt, D. Gut (2003) [Pubmed]
  5. Protective effects of meloxicam on aluminum overload-induced cerebral damage in mice. Jun-Qing, Y., Bei-Zhong, L., Bai-Cheng, H., Qi-Qin, Z. Eur. J. Pharmacol. (2006) [Pubmed]
  6. Cyclooxygenase-2-selective nonsteroidal anti-inflammatory drugs inhibit hepatocyte growth factor/scatter factor-induced angiogenesis. Sengupta, S., Sellers, L.A., Cindrova, T., Skepper, J., Gherardi, E., Sasisekharan, R., Fan, T.P. Cancer Res. (2003) [Pubmed]
  7. The cyclooxygenase system participates in functional mdr1b overexpression in primary rat hepatocyte cultures. Ziemann, C., Schäfer, D., Rüdell, G., Kahl, G.F., Hirsch-Ernst, K.I. Hepatology (2002) [Pubmed]
  8. Effect of cardiovascular comorbidities and concomitant aspirin use on selection of cyclooxygenase inhibitor among rheumatologists. Greenberg, J.D., Bingham, C.O., Abramson, S.B., Reed, G., Sebaldt, R.J., Kremer, J. Arthritis Rheum. (2005) [Pubmed]
  9. Meloxicam. Noble, S., Balfour, J.A. Drugs (1996) [Pubmed]
  10. Comparison of the incidence rates of selected gastrointestinal events reported for patients prescribed celecoxib and meloxicam in general practice in England using prescription-event monitoring (PEM) data. Layton, D., Hughes, K., Harris, S., Shakir, S.A. Rheumatology (Oxford, England) (2003) [Pubmed]
  11. Hyperalgesia due to nerve injury: role of prostaglandins. Syriatowicz, J.P., Hu, D., Walker, J.S., Tracey, D.J. Neuroscience (1999) [Pubmed]
  12. A quantitative approach to measure joint pain in experimental osteoarthritis--evidence of a role for nitric oxide. Castro, R.R., Cunha, F.Q., Silva, F.S., Rocha, F.A. Osteoarthr. Cartil. (2006) [Pubmed]
  13. A single-blind, randomized, controlled trial to assess the efficacy and tolerability of rofecoxib, diclofenac sodium, and meloxicam in patients with acute gouty arthritis. Cheng, T.T., Lai, H.M., Chiu, C.K., Chem, Y.C. Clinical therapeutics. (2004) [Pubmed]
  14. Clinical pharmacokinetics of meloxicam. A cyclo-oxygenase-2 preferential nonsteroidal anti-inflammatory drug. Davies, N.M., Skjodt, N.M. Clinical pharmacokinetics. (1999) [Pubmed]
  15. Meloxicam inhibits osteosarcoma growth, invasiveness and metastasis by COX-2-dependent and independent routes. Naruse, T., Nishida, Y., Hosono, K., Ishiguro, N. Carcinogenesis (2006) [Pubmed]
  16. Articular diffusion of meloxicam after a single oral dose: relationship to cyclo-oxygenase inhibition in synovial cells. Lapicque, F., Vergne, P., Jouzeau, J.Y., Loeuille, D., Gillet, P., Vignon, E., Thomas, P., Velicitat, P., Türck, D., Guillaume, C., Gaucher, A., Bertin, P., Netter, P. Clinical pharmacokinetics. (2000) [Pubmed]
  17. Prevention of cytokine-induced changes in leukocyte adhesion receptors by nonsteroidal antiinflammatory drugs from the oxicam family. García-Vicuña, R., Díaz-González, F., González-Alvaro, I., del Pozo, M.A., Mollinedo, F., Cabañas, C., González-Amaro, R., Sánchez-Madrid, F. Arthritis Rheum. (1997) [Pubmed]
  18. Meloxicam inhibits the growth of colorectal cancer cells. Goldman, A.P., Williams, C.S., Sheng, H., Lamps, L.W., Williams, V.P., Pairet, M., Morrow, J.D., DuBois, R.N. Carcinogenesis (1998) [Pubmed]
  19. Effect of the specific cyclooxygenase-2 inhibitor meloxicam on tumour growth and cachexia in a murine model. Hussey, H.J., Tisdale, M.J. Int. J. Cancer (2000) [Pubmed]
  20. Dissection of metabolic, vascular, and nerve conduction interrelationships in experimental diabetic neuropathy by cyclooxygenase inhibition and acetyl-L-carnitine administration. Pop-Busui, R., Marinescu, V., Van Huysen, C., Li, F., Sullivan, K., Greene, D.A., Larkin, D., Stevens, M.J. Diabetes (2002) [Pubmed]
  21. Comparison of inhibitory effects of meloxicam and diclofenac on human thromboxane biosynthesis after single doses and at steady state. Tegeder, I., Lötsch, J., Krebs, S., Muth-Selbach, U., Brune, K., Geisslinger, G. Clin. Pharmacol. Ther. (1999) [Pubmed]
  22. Rofecoxib: a review of its use in the management of osteoarthritis, acute pain and rheumatoid arthritis. Matheson, A.J., Figgitt, D.P. Drugs (2001) [Pubmed]
  23. The effects of meloxicam, indomethacin or NS-398 on eicosanoid synthesis by fresh human gastric mucosa. Tavares, I.A. Aliment. Pharmacol. Ther. (2000) [Pubmed]
  24. Prostaglandin E2 induces hypoxia-inducible factor-1alpha stabilization and nuclear localization in a human prostate cancer cell line. Liu, X.H., Kirschenbaum, A., Lu, M., Yao, S., Dosoretz, A., Holland, J.F., Levine, A.C. J. Biol. Chem. (2002) [Pubmed]
  25. Meloxicam: selective COX-2 inhibition in clinical practice. Furst, D.E. Semin. Arthritis Rheum. (1997) [Pubmed]
  26. Meloxicam: influence on arachidonic acid metabolism. Part II. In vivo findings. Engelhardt, G., Bögel, R., Schnitzler, C., Utzmann, R. Biochem. Pharmacol. (1996) [Pubmed]
  27. Meloxicam inhibits prostaglandin E(2) generation via cyclooxygenase 2 in the inflammatory site but not that via cyclooxygenase 1 in the stomach. Ogino, K., Hatanaka, K., Kawamura, M., Ohno, T., Harada, Y. Pharmacology (2000) [Pubmed]
  28. Risk of serious upper gastrointestinal and cardiovascular thromboembolic complications with meloxicam. Singh, G., Lanes, S., Triadafilopoulos, G. Am. J. Med. (2004) [Pubmed]
  29. Gastrointestinal safety profile of meloxicam: a meta-analysis and systematic review of randomized controlled trials. Schoenfeld, P. Am. J. Med. (1999) [Pubmed]
  30. Effect of structural modification of enol-carboxamide-type nonsteroidal antiinflammatory drugs on COX-2/COX-1 selectivity. Lazer, E.S., Miao, C.K., Cywin, C.L., Sorcek, R., Wong, H.C., Meng, Z., Potocki, I., Hoermann, M., Snow, R.J., Tschantz, M.A., Kelly, T.A., McNeil, D.W., Coutts, S.J., Churchill, L., Graham, A.G., David, E., Grob, P.M., Engel, W., Meier, H., Trummlitz, G. J. Med. Chem. (1997) [Pubmed]
WikiGenes - Universities