PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 29238904-3 2018 The test compounds fenofibric acid, fenofibrate, and the standard drug diclofenac exhibited binding energies of - 9.0, - 7.2, and - 8.0 kcal mol-1, respectively, against COX-2 and - 7.2, - 7.0, and - 6.5 kcal mol-1, respectively, against COX-1. Diclofenac 71-81 mitochondrially encoded cytochrome c oxidase I Homo sapiens 238-243 20470236-2 2010 As with all NSAIDs, diclofenac exerts its action via inhibition of prostaglandin synthesis by inhibiting cyclooxygenase-1 (COX-1) and cyclooxygenase-2 (COX-2) with relative equipotency. Diclofenac 20-30 mitochondrially encoded cytochrome c oxidase I Homo sapiens 123-128 28179185-6 2018 As a non-steroidal anti-inflammatory drug (NSAID), DS binds to both forms of COX (COX-1 and COX-2) and inhibits the conversion of arachidonic acid into pro-inflammatory prostaglandins by means of chelation. Diclofenac 51-53 mitochondrially encoded cytochrome c oxidase I Homo sapiens 82-87 28179185-8 2018 DS is effective in overcoming pain and inflammation when it inhibits COX-2, but gastrointestinal side effects appear when it inhibits COX-1. Diclofenac 0-2 mitochondrially encoded cytochrome c oxidase I Homo sapiens 134-139 23289871-3 2013 In this study, we tested if topical diclofenac, which inhibits both COX-1 and COX-2, administration rendered prostate tumor cells sensitize to the effects of radiation. Diclofenac 36-46 mitochondrially encoded cytochrome c oxidase I Homo sapiens 68-73 22091869-0 2011 Binding of ibuprofen, ketorolac, and diclofenac to COX-1 and COX-2 studied by saturation transfer difference NMR. Diclofenac 37-47 mitochondrially encoded cytochrome c oxidase I Homo sapiens 51-56 22091869-2 2011 Here we report the application of STD-NMR to characterize the binding of the anti-inflammatory drugs ibuprofen, diclofenac, and ketorolac to COX-1 and COX-2. Diclofenac 112-122 mitochondrially encoded cytochrome c oxidase I Homo sapiens 141-146 21056807-14 2010 Diclofenac, with its balanced COX-1 and COX-2 inhibitory profile, may pose less risk of postoperative bleeding than nonsteroidal antiinflammatory drugs (NSAIDs) such as ketorolac and ASA, which predominantly inhibit COX-1. Diclofenac 0-10 mitochondrially encoded cytochrome c oxidase I Homo sapiens 30-35 21056807-14 2010 Diclofenac, with its balanced COX-1 and COX-2 inhibitory profile, may pose less risk of postoperative bleeding than nonsteroidal antiinflammatory drugs (NSAIDs) such as ketorolac and ASA, which predominantly inhibit COX-1. Diclofenac 0-10 mitochondrially encoded cytochrome c oxidase I Homo sapiens 216-221 24796327-6 2014 RESULTS: The half-maximal inhibitory concentration (IC50) of diclofenac, bromfenac, and amfenac was 55.5, 5.56, and 15.3 nM for human COX-1, and 30.7, 7.45, and 20.4 nM for human COX-2, respectively. Diclofenac 61-71 mitochondrially encoded cytochrome c oxidase I Homo sapiens 134-139 20817448-4 2011 The assay was validated using four COX inhibitors, celecoxib, indomethacin, resveratrol, and diclofenac that exhibit different selectivities towards COX-1 and COX-2. Diclofenac 93-103 mitochondrially encoded cytochrome c oxidase I Homo sapiens 149-154 18434566-0 2008 Comparative inhibitory activity of etoricoxib, celecoxib, and diclofenac on COX-2 versus COX-1 in healthy subjects. Diclofenac 62-72 mitochondrially encoded cytochrome c oxidase I Homo sapiens 89-94 18477264-1 2008 WHAT IS ALREADY KNOWN ABOUT THIS SUBJECT: Diclofenac, a nonselective nonsteroidal anti-inflammatory drug,, exerts analgesic action both in the peripheral tissues and in the central nervous system by inhibiting cyclooxygenase enzymes COX-1/2, but central nervous system penetration of diclofenac has not been evaluated in humans. Diclofenac 42-52 mitochondrially encoded cytochrome c oxidase I Homo sapiens 233-240 18477264-2 2008 WHAT THIS STUDY ADDS: Diclofenac penetrates the cerebrospinal fluid rapidly, and after a single intravenous dose of 1 mg kg(-1), sufficient concentrations to inhibit COX-1/2 are sustained for up to 4 h. AIMS: The primary aim was to study the cerebrospinal fluid (CSF) penetration of intravenous diclofenac in children. Diclofenac 22-32 mitochondrially encoded cytochrome c oxidase I Homo sapiens 166-173 20648923-9 2010 Furthermore, compared to ASA and to diclofenac (Diclo, CAS 15307-79-6), the COX-1 and COX-2 mRNA expressions were influenced differently by STW 33-I and fraction E. ASA and Diclo inhibited both the COX-1 and COX-2 mRNA expressions, whereas STW 33-I and its fraction E increased the COX-1 mRNA expression. Diclofenac 173-178 mitochondrially encoded cytochrome c oxidase I Homo sapiens 76-81 12534640-10 2003 Marked diclofenac mediated inhibition of COX-1- and COX-2 activity was detected in all individuals independent of CYP2C9 genotype. Diclofenac 7-17 mitochondrially encoded cytochrome c oxidase I Homo sapiens 41-46 15107131-3 2004 Aim of this study was to examine the influence of the COX-1 inhibiting NSAIDs, diclofenac and metamizol on platelet activation and leukocyte-platelet complexes, in vitro. Diclofenac 79-89 mitochondrially encoded cytochrome c oxidase I Homo sapiens 54-59 12966366-8 2003 Maximal plasma concentrations of diclofenac after oral administration of aceclofenac (0.39 micromol/L) or diclofenac (1.28 micromol/L) were sufficient for a greater than 97% inhibition of COX-2 (50% inhibitory concentration, 0.024 micromol/L) and a 46% (aceclofenac treatment) or 82% inhibition (diclofenac treatment) of COX-1 (50% inhibitory concentration, 0.43 micromol/L). Diclofenac 33-43 mitochondrially encoded cytochrome c oxidase I Homo sapiens 321-326 12966366-8 2003 Maximal plasma concentrations of diclofenac after oral administration of aceclofenac (0.39 micromol/L) or diclofenac (1.28 micromol/L) were sufficient for a greater than 97% inhibition of COX-2 (50% inhibitory concentration, 0.024 micromol/L) and a 46% (aceclofenac treatment) or 82% inhibition (diclofenac treatment) of COX-1 (50% inhibitory concentration, 0.43 micromol/L). Diclofenac 106-116 mitochondrially encoded cytochrome c oxidase I Homo sapiens 321-326 12966366-8 2003 Maximal plasma concentrations of diclofenac after oral administration of aceclofenac (0.39 micromol/L) or diclofenac (1.28 micromol/L) were sufficient for a greater than 97% inhibition of COX-2 (50% inhibitory concentration, 0.024 micromol/L) and a 46% (aceclofenac treatment) or 82% inhibition (diclofenac treatment) of COX-1 (50% inhibitory concentration, 0.43 micromol/L). Diclofenac 106-116 mitochondrially encoded cytochrome c oxidase I Homo sapiens 321-326 12966366-9 2003 Moreover, ex vivo COX-1-dependent thromboxane B(2) synthesis was inhibited significantly less by aceclofenac than by diclofenac. Diclofenac 117-127 mitochondrially encoded cytochrome c oxidase I Homo sapiens 18-23 11556519-14 2001 Diclofenac strongly inhibited both COX-1 and COX-2 with IC50 values of 0.6 and 0.04 microM, respectively. Diclofenac 0-10 mitochondrially encoded cytochrome c oxidase I Homo sapiens 35-40 11874389-8 2002 However, after oral intake, ibuprofen inhibited ex vivo COX-2 by 80% whereas diclofenac inhibited COX-1 by 70%. Diclofenac 77-87 mitochondrially encoded cytochrome c oxidase I Homo sapiens 98-103 11874389-10 2002 Using in vitro dose--response curves, the in vivo inhibitory potency of diclofenac was estimated adequately from its circulating concentration ([-0.18, 0.21] for COX-1 and [-0.13, -0.03] for COX-2) but this was not the case for ibuprofen on COX-2 ([-0.14, 0.27]) and meloxicam on COX-1 ([0.31, 1.05]). Diclofenac 72-82 mitochondrially encoded cytochrome c oxidase I Homo sapiens 162-167 11874389-10 2002 Using in vitro dose--response curves, the in vivo inhibitory potency of diclofenac was estimated adequately from its circulating concentration ([-0.18, 0.21] for COX-1 and [-0.13, -0.03] for COX-2) but this was not the case for ibuprofen on COX-2 ([-0.14, 0.27]) and meloxicam on COX-1 ([0.31, 1.05]). Diclofenac 72-82 mitochondrially encoded cytochrome c oxidase I Homo sapiens 280-285 10381057-13 1999 Indomethacin and diclofenac were the most potent inhibitors of COX-1 (IC50 = 0.063 microM and 0.611 microM, respectively) and COX-2 isoforms (IC50 = 0.48 microM and IC50 = 0.63 microM, respectively). Diclofenac 17-27 mitochondrially encoded cytochrome c oxidase I Homo sapiens 63-68 11153163-10 2000 COX-1 was more inhibited by indomethacin and piroxicam and COX-2 by 6-MNA (active metabolite of nabumetone), diclofenac and ibuprofen. Diclofenac 109-119 mitochondrially encoded cytochrome c oxidase I Homo sapiens 0-5 11552612-2 2000 The advantages of VOLTAREN are: efficacy in all NSAID indications, good tolerability, favourable COX-2/COX-1 ratio, the wide range of drug forms, long treatment experience and extremely acceptable cost-benefit ratio. Diclofenac 18-26 mitochondrially encoded cytochrome c oxidase I Homo sapiens 103-108 10391671-2 1999 Nonsteroidal antiinflammatory drugs (NSAIDs) such as ibuprofen and diclofenac inhibit both COX-1 and COX-2. Diclofenac 67-77 mitochondrially encoded cytochrome c oxidase I Homo sapiens 91-96 10381057-16 1999 Aspirin and piroxicam were about 8 times more active against COX-1 than COX-2, indomethacin was 7 times more active, and diclofenac was an equipotent inhibitor of COX-1 and COX-2. Diclofenac 121-131 mitochondrially encoded cytochrome c oxidase I Homo sapiens 163-168 10340919-3 1999 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). Diclofenac 182-192 mitochondrially encoded cytochrome c oxidase I Homo sapiens 9-14 10340919-3 1999 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). Diclofenac 247-257 mitochondrially encoded cytochrome c oxidase I Homo sapiens 9-14