PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
31985369-9	2020	Hence, in vitro COX-2 inhibitory assay performed for epicatechin, daidzein and compared with known analgesic agent diclofenac revealed a pronounced dose dependent inhibitory activity.	Diclofenac	115-125	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	16-21	
33964802-4	2021	Based on docking results, COX-2 inhibitors were designed and 6o appears as the most selective derivative which showed an improved selective index compared with indomethacin (IND) and diclofenac (DCF), used as reference drugs.	Diclofenac	183-193	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	26-31	
33964802-4	2021	Based on docking results, COX-2 inhibitors were designed and 6o appears as the most selective derivative which showed an improved selective index compared with indomethacin (IND) and diclofenac (DCF), used as reference drugs.	Diclofenac	195-198	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	26-31	
31916080-4	2020	Among NSAIDs, diclofenac appeared to be associated with a relatively higher risk of MI, similar to that of rofecoxib, compatible with the drug"s high COX-2 inhibitory potency.	Diclofenac	14-24	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	150-155	
31878864-7	2020	RESULTS: Briefly, the COX-2 inhibitory relative activity was found to be in between the range of 80-92 % (Diclofenac showed 84 %, IC50 0.95 microM).	Diclofenac	106-116	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	22-27	
28870762-2	2018	Diclofenac sodium (DS), one of these NSAIDs, has a high specificity for arachidonic acid-degrading cyclooxygenase (COX)-2 enzymes.	Diclofenac	0-17	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	115-121	
28179185-3	2018	The mechanism of action of DS operates by way of cyclooxygenase (COX) inhibition.	Diclofenac	27-29	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	65-68	
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 II	Homo sapiens	77-80	
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 II	Homo sapiens	92-97	
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 II	Homo sapiens	69-74	
30083389-7	2018	Furthermore, a strong correlation was found between pain relief observed in patients as well as celecoxib- and diclofenac-induced decrease in prostaglandins after 6 h. The findings presented reveal insights about drug-induced modulation of cellular networks in a whole-body context, thereby describing complex pharmacokinetic/pharmacodynamic behavior of COX-2 and 5-LOX inhibitors in therapeutic situations.	Diclofenac	111-121	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	354-365	
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 II	Homo sapiens	170-175	
29235601-7	2018	Molecular docking studies with COX-2 reveal that complexes 1 and 2 having naproxen and diclofenac ligands exhibit stronger interactions with COX-2 than their respective free NSAIDs and these results are in good agreement with their relative experimentally observed COX inhibition as well as anti-proliferative activities.	Diclofenac	87-97	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	31-36	
29235601-7	2018	Molecular docking studies with COX-2 reveal that complexes 1 and 2 having naproxen and diclofenac ligands exhibit stronger interactions with COX-2 than their respective free NSAIDs and these results are in good agreement with their relative experimentally observed COX inhibition as well as anti-proliferative activities.	Diclofenac	87-97	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	141-146	
28870762-2	2018	Diclofenac sodium (DS), one of these NSAIDs, has a high specificity for arachidonic acid-degrading cyclooxygenase (COX)-2 enzymes.	Diclofenac	19-21	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	115-121	
27687548-0	2016	NSAIDs diclofenac, indomethacin, and meloxicam highly upregulate expression of ICAM-1 and COX-2 induced by X-irradiation in human endothelial cells.	Diclofenac	7-17	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	90-95	
27687548-10	2016	Indomethacin, diclofenac, and meloxicam highly upregulated radiation-induced expression of ICAM-1 and COX-2.	Diclofenac	14-24	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	102-107	
27687548-13	2016	CONCLUSION: Indomethacin, diclofenac, and meloxicam highly upregulated radiation-induced expression of ICAM-1 and COX-2 in HUVECs, which suggests that use of these NSAIDs may increase the effects of ionizing radiation and affect the risk of MI after radiation exposure to the heart.	Diclofenac	26-36	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	114-119	
23289871-0	2013	Inhibition of COX-2 expression by topical diclofenac enhanced radiation sensitivity via enhancement of TRAIL in human prostate adenocarcinoma xenograft model.	Diclofenac	42-52	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	14-19	
27548780-7	2016	COX-2 inhibition activity of diclofenac was retained when conjugated to DKP.	Diclofenac	29-39	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	0-5	
27014880-3	2016	In fact, diclofenac"s increased effect on spinal nociception and chronic neuro-inflammatory pain may be referred to: 1) its synergistic effects on peroxisome proliferator-activated receptor-gamma (PPAR- gamma) activation and prostaglandin synthesis inhibition (COX-2 inhibition); 2) its capacity of suppressing neuronal hyperexcitability through the blockage of neuronal K+ channels in a concentration-dependant manner; and 3) its facility to cross the blood-brain barrier.	Diclofenac	9-19	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	261-266	
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 II	Homo sapiens	179-184	
27831630-2	2016	Data collected during the last 10 years reported a dose-duration dependent increasing of cardiovascular risk associated with the use of diclofenac, supporting the evidence of a close association with the degree of COX-2 inhibition achieved in vivo.	Diclofenac	136-146	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	214-219	
27831630-6	2016	Today, new low-dosage diclofenac formulations are available, allowing to reduce the systemic exposure, the degree of COX-2 inhibition and possibly the risk of occurrence of cardiovascular events.	Diclofenac	22-32	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	117-122	
26823679-3	2016	DCF, which is a potent inhibitor of COX-2 and prostaglandin E2 synthesis, displays a range of effects on the immune system, the angiogenic cascade, chemo- and radio-sensitivity and tumour metabolism.	Diclofenac	0-3	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	36-41	
25378670-8	2014	Comparing the different COX-2 inhibitors, the HR was driven by new use of older traditional COX-2 inhibitors (1.42, 95% CI: 1.14-1.78) among which it was 1.53 (95% CI: 1.02-2.28) for etodolac and 1.28 (95% CI: 0.98-1.68) for diclofenac.	Diclofenac	225-235	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	24-29	
25378670-8	2014	Comparing the different COX-2 inhibitors, the HR was driven by new use of older traditional COX-2 inhibitors (1.42, 95% CI: 1.14-1.78) among which it was 1.53 (95% CI: 1.02-2.28) for etodolac and 1.28 (95% CI: 0.98-1.68) for diclofenac.	Diclofenac	225-235	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	92-97	
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 II	Homo sapiens	78-83	
23289871-7	2013	In addition, we assessed the tumor volumes of xenograft LNCaP-COX-2 cells treated with topical diclofenac with or without radiation therapy (RT).	Diclofenac	95-105	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	62-67	
23289871-8	2013	RESULTS: LNCaP-COX-2 and LNCaP-Neo cell lines experienced cytotoxic effects of diclofenac in a dose related manner.	Diclofenac	79-89	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	15-20	
23289871-10	2013	Furthermore, the addition of diclofenac sensitized LNCaP-COX-2 not but LNCaP-Neo cells to the cytocidal effects of radiation.	Diclofenac	29-39	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	57-62	
23289871-11	2013	In LNCaP-COX-2 cells, diclofenac enhanced radiation-induced apoptosis compared with RT alone.	Diclofenac	22-32	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	9-14	
23289871-14	2013	CONCLUSIONS: These in vitro and in vivo findings suggest that conventional COX inhibitor, diclofenac enhances the effect of RT on prostate cancer cells that express COX-2.	Diclofenac	90-100	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	165-170	
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 II	Homo sapiens	61-66	
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 II	Homo sapiens	151-156	
22091869-3	2011	Using well-studied COX inhibitors and by comparing STD signals with crystallographic structures, we show that there is a relation between the orientations of ibuprofen and diclofenac in the COX-2 active site and the relative STD responses detected in the NMR experiments.	Diclofenac	172-182	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	190-195	
20092437-3	2010	Large retrospective analyses of clinical data have repeatedly shown that diclofenac, similar as some selective COX-2 inhibitors, increases the propensity to experience adverse cardiovascular and atherothrombotic events.	Diclofenac	73-83	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	111-116	
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 II	Homo sapiens	159-164	
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 II	Homo sapiens	40-45	
20237495-3	2010	The NSAID diclofenac is an inhibitor of COX-2; however, its mode of action in cutaneous epithelial cancer cells is largely unknown.	Diclofenac	10-20	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	40-45	
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 II	Homo sapiens	152-157	
21830840-1	2011	BACKGROUND: Naproxen, ibuprofen and diclofenac are frequently used as comparators in randomized controlled trials (RCTs) on the safety and efficacy of cyclooxygenase (COX)-2 inhibitors.	Diclofenac	36-46	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	151-173	
20631416-5	2010	These are a putative cyclooxygenase-3 which is a variant of cyclooxygenase-1 and derives from the same gene, and a COX-2 variant, induced with diclofenac, which may be involved in the resolution of inflammation.	Diclofenac	143-153	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	115-120	
20092437-5	2010	The reasons for this novel side-effect of diclofenac may be based on the specific pharmacology of diclofenac, which, similar to selective COX-2 inhibitors, alters vascular levels of platelet active prostaglandins in a way that favours arterial thrombosis.	Diclofenac	42-52	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	138-143	
20092437-5	2010	The reasons for this novel side-effect of diclofenac may be based on the specific pharmacology of diclofenac, which, similar to selective COX-2 inhibitors, alters vascular levels of platelet active prostaglandins in a way that favours arterial thrombosis.	Diclofenac	98-108	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	138-143	
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 II	Homo sapiens	86-91	
19841157-5	2010	Oral diclofenac inhibited platelet aggregation, cyclooxygenase-1 (COX-1), and COX-2.	Diclofenac	5-15	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	78-83	
19841157-6	2010	Topical diclofenac did not inhibit platelet aggregation and inhibited COX-1 and COX-2 less than oral diclofenac.	Diclofenac	8-18	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	80-85	
19602986-4	2009	The hazard might also extend to traditional NSAIDs, which are relatively selective for COX-2, such as diclofenac, meloxicam, and etodolac.	Diclofenac	102-112	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	87-92	
20096163-5	2009	Herein, we give an overview about actinic keratosis focusing on treatment with the COX-2 inhibitor diclofenac 3 % gel and summarize current concepts of its antineoplastic mode of action.	Diclofenac	99-109	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	83-88	
18674517-9	2008	Molecular modeling of selective thiopheneacetic acid derivatives to the active site of human COX-2 suggested similar binding properties as Lumiracoxib and Diclofenac.	Diclofenac	155-165	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	93-98	
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 II	Homo sapiens	76-81	
17164136-4	2007	In contrast, the tNSAIDs meloxicam, nimesulide and diclofenac (which are from 18- to 29-fold more potent towards COX-2 in vitro) and coxibs (i.e. celecoxib, valdecoxib, rofecoxib, etoricoxib and lumiracoxib, which are from 30- to 433-fold more potent towards COX-2 in vitro) should be comprised into the cluster of COX-2 inhibitors.	Diclofenac	51-61	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	113-118	
17965743-8	2007	CONCLUSIONS AND IMPLICATIONS: Diclofenac and lumiracoxib, in addition to being COX unselective and highly COX-2 selective inhibitors, respectively, displayed a previously unknown pharmacological activity, namely TP receptor antagonism.	Diclofenac	30-40	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	106-111	
17164136-4	2007	In contrast, the tNSAIDs meloxicam, nimesulide and diclofenac (which are from 18- to 29-fold more potent towards COX-2 in vitro) and coxibs (i.e. celecoxib, valdecoxib, rofecoxib, etoricoxib and lumiracoxib, which are from 30- to 433-fold more potent towards COX-2 in vitro) should be comprised into the cluster of COX-2 inhibitors.	Diclofenac	51-61	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	259-264	
17164136-4	2007	In contrast, the tNSAIDs meloxicam, nimesulide and diclofenac (which are from 18- to 29-fold more potent towards COX-2 in vitro) and coxibs (i.e. celecoxib, valdecoxib, rofecoxib, etoricoxib and lumiracoxib, which are from 30- to 433-fold more potent towards COX-2 in vitro) should be comprised into the cluster of COX-2 inhibitors.	Diclofenac	51-61	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	259-264	
15133778-9	2004	CONCLUSIONS: Patients on the COX-2 specific inhibitors (celecoxib and rofecoxib) were significantly less likely to switch their therapy than patients on NS-NSAIDS (ibuprofen, naproxen and diclofenac).	Diclofenac	188-198	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	29-34	
18605234-14	2007	Considering the cardiovascular effects of COX-2 selective inhibitors, the combination of diclofenac and misoprostol could represent a safer and effective alternative for patients with pain.	Diclofenac	89-99	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	42-47	
15555544-7	2004	By EPR spin trapping, COX-2 inhibitors, ibuprofen, and diclofenac, exhibited a dose-dependent inhibiting effect (10 and 100muM) on the EPR signal appearance.	Diclofenac	55-65	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	22-27	
16934053-6	2006	A parallel increase in the prescription of diclofenac and ibuprofen was also noted, suggesting that prescribers were prescribing these medications as alternatives to COX-2 inhibitors.	Diclofenac	43-53	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	166-171	
12852704-1	2003	BACKGROUND: Traditional nonsteroidal anti-inflammatory drugs (NSAIDs) such as diclofenac, ibuprofen, naproxen, and related agents are nonselective inhibitors of both cyclooxygenase-1 (COX-1) and COX-2, which catalyze prostaglandin synthesis.	Diclofenac	78-88	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	195-200	
14655004-5	2003	The clinical efficacy of the marketed COX-2 inhibitors has been proved in large phase III clinical trials in comparison to both placebo and classical NSAIDs (e.g. diclofenac, naproxen).	Diclofenac	163-173	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	38-43	
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 II	Homo sapiens	188-193	
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 II	Homo sapiens	188-193	
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 II	Homo sapiens	188-193	
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 II	Homo sapiens	97-102	
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 II	Homo sapiens	52-57	
11874389-7	2002	The ratios of IC50s and, at best, of IC80s revealed diclofenac and meloxicam as selective COX-2 inhibitors and ibuprofen as a preferential COX-1 inhibitor in vitro.	Diclofenac	52-62	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	90-95	
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 II	Homo sapiens	191-196	
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 II	Homo sapiens	241-246	
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 II	Homo sapiens	45-50	
11028250-0	2000	Comparative inhibitory activity of rofecoxib, meloxicam, diclofenac, ibuprofen, and naproxen on COX-2 versus COX-1 in healthy volunteers.	Diclofenac	57-67	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	96-101	
11742186-6	2001	Co-administration of the COX-2 selective NSAID, celecoxib, and low-dose aspirin, is associated with the same risk for upper gastrointestinal ulcer complications alone and combined with symptomatic ulcers, as the non-selective NSAIDs, ibuprofen and diclofenac.	Diclofenac	248-258	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	25-30	
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 II	Homo sapiens	59-64	
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 II	Homo sapiens	101-106	
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 II	Homo sapiens	126-131	
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 II	Homo sapiens	173-178	
8718891-1	1996	The steady state tryptophan fluorescence of apo-human cyclooxygenase-2 (hCox-2) is quenched approximately 40%-50% by the slow binding inhibitors diclofenac, indomethacin, ketoprofen, NS-398, and DuP-697.	Diclofenac	145-155	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	72-78	
9831331-3	1998	Meloxicam, etodolac and diclofenac also showed high COX-2 selectivity.	Diclofenac	24-34	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	52-57	
34182020-5	2021	Thus, the relative COX-2 selectivity of traditional NSAIDs correlates with their cardiovascular risk profile, being more favorable for non-selective NSAIDs, such as naproxen and low-dose ibuprofen, and less favorable for more COX-2 selective agents, such as diclofenac.	Diclofenac	258-268	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	19-24	
33813964-6	2021	The computational finding supported those of in vitro, where the pyrazolylpyrazolines interacted with the COX-2 enzyme in a similar orientation to that of Celecoxib, while chlacones were found to exhibit similar orientation to that of Diclofenac.	Diclofenac	235-245	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	106-111	
35585779-7	2022	The "traditional" NSAID diclofenac is as COX-2 selective as celecoxib and increases cardiovascular risk dose-dependently.	Diclofenac	24-34	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	41-46	
34568119-7	2021	The acceptance of Diclofenac is partly attributed to being a potent COX-2 inhibitor with the lowest IC50 and its rapid onset of action at lowest effective dose.	Diclofenac	18-28	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	68-73	
35159907-2	2022	We explored and compared the loading/release ability of diclofenac (COX-2 antagonist), in both undoped- and luminescent Terbium3+ (Tb3+)-doped citrate-coated carbonated apatite nanoparticles at different temperatures (25, 37, 40  C) and pHs (7.4, 5.2).	Diclofenac	56-66	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	68-73	
35159907-4	2022	Biological effects of diclofenac-loaded-nanoparticles were monitored in an in vitro osteoblast"s cytokine-induced inflammation model by evaluating COX-2 mRNA expression and production of PGE2.	Diclofenac	22-32	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	147-152	
35159907-10	2022	In addition, diclofenac release increased COX-2 mRNA expression and decreased PGE2 production in an in vitro inflammation model.	Diclofenac	13-23	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	42-47