PMID-sentid	Pub_year	Sent_text	compound_name	comp_offset	prot_official_name	organism	prot_offset
18437583-13	2008	Recent studies showed that the use of colloidal nanoparticle formulations and the potent COX 2 inhibitor bromfenac may enhance NSAID efficacy in eye preparations.	bromfenac	105-114	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	89-94
34820575-4	2022	The inhibitory effect of bromfenac on TGF-beta2-induced EMT was also verified on a primary lens epithelial cell model using human anterior capsules.	bromfenac	25-34	transforming growth factor beta 2	Homo sapiens	38-47
17720067-6	2007	In addition, COX-1 (homeostatic) and COX-2 (inducible) inhibitory activities of nepafenac, amfenac, ketorolac, and bromfenac were determined via the in vitro measurement of prostaglandin E(2) (PGE(2)) inhibition.	bromfenac	115-124	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	13-18
17720067-6	2007	In addition, COX-1 (homeostatic) and COX-2 (inducible) inhibitory activities of nepafenac, amfenac, ketorolac, and bromfenac were determined via the in vitro measurement of prostaglandin E(2) (PGE(2)) inhibition.	bromfenac	115-124	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	37-42
16846546-11	2006	CONCLUSIONS: Ketorolac is relatively COX-1 selective while bromfenac is potently selective for COX-2 over COX-1.	bromfenac	59-68	cytochrome c oxidase subunit II	Oryctolagus cuniculus	95-100
16846546-11	2006	CONCLUSIONS: Ketorolac is relatively COX-1 selective while bromfenac is potently selective for COX-2 over COX-1.	bromfenac	59-68	cytochrome c oxidase subunit I	Oryctolagus cuniculus	106-111
34519442-4	2022	Lens-treated eyes show a continuous, therapeutically relevant bromfenac tear concentration of 256.4 +- 23.1 microg mL-1 for 8 days.	bromfenac	62-71	L1 cell adhesion molecule	Mus musculus	115-119
34519442-5	2022	Bromday (bromfenac ophthalmic solution, 0.09%, Bausch+Lomb) topical drops exhibit a quick peak concentration of 269.3 +- 85.7 microg mL-1 and 100 min duration.	bromfenac	9-18	L1 cell adhesion molecule	Mus musculus	133-137
34820575-7	2022	In conclusion, bromfenac can inhibit TGF-beta2-induced cell migration and the EMT of LECs via ERK/GSK-3beta/Snail signaling.	bromfenac	15-24	transforming growth factor beta 2	Homo sapiens	37-46
34820575-7	2022	In conclusion, bromfenac can inhibit TGF-beta2-induced cell migration and the EMT of LECs via ERK/GSK-3beta/Snail signaling.	bromfenac	15-24	mitogen-activated protein kinase 1	Homo sapiens	94-97
34820575-7	2022	In conclusion, bromfenac can inhibit TGF-beta2-induced cell migration and the EMT of LECs via ERK/GSK-3beta/Snail signaling.	bromfenac	15-24	glycogen synthase kinase 3 alpha	Homo sapiens	98-107
34820575-7	2022	In conclusion, bromfenac can inhibit TGF-beta2-induced cell migration and the EMT of LECs via ERK/GSK-3beta/Snail signaling.	bromfenac	15-24	snail family transcriptional repressor 1	Homo sapiens	108-113
32209318-3	2020	Bromfenac has shown promise in inhibiting the COX-2 enzymatic pathway that partially causes the inflammatory cascade which contributes to the precipitation of DME.	bromfenac	0-9	cytochrome c oxidase subunit II	Oryctolagus cuniculus	46-51
3497637-3	1987	In dogs bromfenac when given orally was 5.8 times more potent than zomepirac in blocking the nociceptive response to bradykinin.	bromfenac	8-17	kininogen 1	Canis lupus familiaris	117-127
33727659-6	2021	Bromfenac also significantly decreased vascular endothelial growth factor level (P = 0.0077), as well as monocyte chemoattractant protein-1 level (P = 0.013), which was elevated for a prolonged period after phacoemulsification.	bromfenac	0-9	vascular endothelial growth factor A	Homo sapiens	39-73
35213965-8	2022	Finally, the FDA-approved drugs bilastine, bromfenac, and fenofibric acid are suggested as potential and lead FFA1 agonists.	bromfenac	43-52	free fatty acid receptor 1	Homo sapiens	110-114
32705205-0	2020	Protective effect of bromfenac sodium on femtosecond laser-assisted cataract surgery via modulating cyclooxygenase-2 expression.	bromfenac	21-37	prostaglandin-endoperoxide synthase 2	Homo sapiens	100-116
31815452-4	2020	(Driscoll, et al 2018) Here cytochrome P450 (CYP) and UDP-glucuronosyltransferase (UGT) reaction phenotyping experiments using recombinant enzymes were performed on bromfenac and BI to identify the CYP and UGT enzymes responsible for bromfenac"s metabolism and bioactivation.	bromfenac	165-174	cytochrome P450 family 4 subfamily F member 3	Homo sapiens	28-43
32037749-5	2020	Compared to the control group, at 1 month after surgery, the bromfenac group showed slightly better best-corrected visual acuity (0.12 +- 0.12 vs. 0.32 +- 0.42, p = 0.142), lower central macular thickness (265.58 +- 31.28 vs. 314.15 +- 76.11 mum, p < 0.001), and lower macular volume (8.46 +- 0.60 vs. 9.14 +- 1.53 mm3, p = 0.022).	bromfenac	61-70	latexin	Homo sapiens	242-245
31815452-5	2020	It was determined that UGT2B7 converts bromfenac to BI, and that while CYP2C8, CYP2C9 and CYP2C19 catalyze the hydroxylation of bromfenac, only CYP2C9 forms thioether adducts when incubated with NAC or GSH as trapping agents.	bromfenac	52-54	UDP glucuronosyltransferase family 2 member B7	Homo sapiens	23-29
31815452-5	2020	It was determined that UGT2B7 converts bromfenac to BI, and that while CYP2C8, CYP2C9 and CYP2C19 catalyze the hydroxylation of bromfenac, only CYP2C9 forms thioether adducts when incubated with NAC or GSH as trapping agents.	bromfenac	128-137	UDP glucuronosyltransferase family 2 member B7	Homo sapiens	23-29
31815452-4	2020	(Driscoll, et al 2018) Here cytochrome P450 (CYP) and UDP-glucuronosyltransferase (UGT) reaction phenotyping experiments using recombinant enzymes were performed on bromfenac and BI to identify the CYP and UGT enzymes responsible for bromfenac"s metabolism and bioactivation.	bromfenac	165-174	UDP glucuronosyltransferase family 1 member A complex locus	Homo sapiens	54-81
31815452-5	2020	It was determined that UGT2B7 converts bromfenac to BI, and that while CYP2C8, CYP2C9 and CYP2C19 catalyze the hydroxylation of bromfenac, only CYP2C9 forms thioether adducts when incubated with NAC or GSH as trapping agents.	bromfenac	128-137	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	71-77
31815452-4	2020	(Driscoll, et al 2018) Here cytochrome P450 (CYP) and UDP-glucuronosyltransferase (UGT) reaction phenotyping experiments using recombinant enzymes were performed on bromfenac and BI to identify the CYP and UGT enzymes responsible for bromfenac"s metabolism and bioactivation.	bromfenac	165-174	UDP glucuronosyltransferase family 1 member A complex locus	Homo sapiens	83-86
31815452-4	2020	(Driscoll, et al 2018) Here cytochrome P450 (CYP) and UDP-glucuronosyltransferase (UGT) reaction phenotyping experiments using recombinant enzymes were performed on bromfenac and BI to identify the CYP and UGT enzymes responsible for bromfenac"s metabolism and bioactivation.	bromfenac	179-181	UDP glucuronosyltransferase family 1 member A complex locus	Homo sapiens	54-81
31815452-5	2020	It was determined that UGT2B7 converts bromfenac to BI, and that while CYP2C8, CYP2C9 and CYP2C19 catalyze the hydroxylation of bromfenac, only CYP2C9 forms thioether adducts when incubated with NAC or GSH as trapping agents.	bromfenac	128-137	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	79-85
31815452-4	2020	(Driscoll, et al 2018) Here cytochrome P450 (CYP) and UDP-glucuronosyltransferase (UGT) reaction phenotyping experiments using recombinant enzymes were performed on bromfenac and BI to identify the CYP and UGT enzymes responsible for bromfenac"s metabolism and bioactivation.	bromfenac	179-181	UDP glucuronosyltransferase family 1 member A complex locus	Homo sapiens	83-86
31815452-4	2020	(Driscoll, et al 2018) Here cytochrome P450 (CYP) and UDP-glucuronosyltransferase (UGT) reaction phenotyping experiments using recombinant enzymes were performed on bromfenac and BI to identify the CYP and UGT enzymes responsible for bromfenac"s metabolism and bioactivation.	bromfenac	234-243	UDP glucuronosyltransferase family 1 member A complex locus	Homo sapiens	54-81
31815452-5	2020	It was determined that UGT2B7 converts bromfenac to BI, and that while CYP2C8, CYP2C9 and CYP2C19 catalyze the hydroxylation of bromfenac, only CYP2C9 forms thioether adducts when incubated with NAC or GSH as trapping agents.	bromfenac	128-137	cytochrome P450 family 2 subfamily C member 19	Homo sapiens	90-97
31815452-5	2020	It was determined that UGT2B7 converts bromfenac to BI, and that while CYP2C8, CYP2C9 and CYP2C19 catalyze the hydroxylation of bromfenac, only CYP2C9 forms thioether adducts when incubated with NAC or GSH as trapping agents.	bromfenac	128-137	synuclein alpha	Homo sapiens	195-198
31815452-7	2020	Reaction phenotyping experiments with BI and recombinant CYP enzymes indicated that CYPs 1A2, 2B6, 2C8, 2C9, 2C19, 2D6 and 3A4 were responsible for the formation of an aliphatic hydroxylated metabolite.	bromfenac	38-40	cytochrome P450 family 1 subfamily A member 2	Homo sapiens	84-97
31815452-10	2020	Through time-dependent inhibition (TDI) experiments, it was revealed that BI can cause an IC50 shift in CYP1A2 and CYP3A4.	bromfenac	74-76	cytochrome P450 family 1 subfamily A member 2	Homo sapiens	104-110
31815452-10	2020	Through time-dependent inhibition (TDI) experiments, it was revealed that BI can cause an IC50 shift in CYP1A2 and CYP3A4.	bromfenac	74-76	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	115-121
31815452-4	2020	(Driscoll, et al 2018) Here cytochrome P450 (CYP) and UDP-glucuronosyltransferase (UGT) reaction phenotyping experiments using recombinant enzymes were performed on bromfenac and BI to identify the CYP and UGT enzymes responsible for bromfenac"s metabolism and bioactivation.	bromfenac	234-243	UDP glucuronosyltransferase family 1 member A complex locus	Homo sapiens	83-86
31815452-5	2020	It was determined that UGT2B7 converts bromfenac to BI, and that while CYP2C8, CYP2C9 and CYP2C19 catalyze the hydroxylation of bromfenac, only CYP2C9 forms thioether adducts when incubated with NAC or GSH as trapping agents.	bromfenac	39-48	UDP glucuronosyltransferase family 2 member B7	Homo sapiens	23-29
30908581-0	2019	Bromfenac Inhibits TGF-beta1-Induced Fibrotic Effects in Human Pterygium and Conjunctival Fibroblasts.	bromfenac	0-9	transforming growth factor beta 1	Homo sapiens	19-28
31534309-7	2019	Bromfenac was well tolerated when given alone or in combination with intravitreal anti-vascular endothelial growth factor agents, topical corticosteroids, or topical mast-cell stabilizers.	bromfenac	0-9	vascular endothelial growth factor A	Homo sapiens	87-121
30908581-5	2019	Results: Bromfenac suppressed the TGF-beta1-induced protein expression of FN (0.59 +- 0.07 folds, P = 0.008), COL3 (0.48 +- 0.08 folds, P = 0.001), and alpha-SMA (0.61 +- 0.03 folds, P = 0.008) in HPFs.	bromfenac	9-18	transforming growth factor beta 1	Homo sapiens	34-43
30908581-5	2019	Results: Bromfenac suppressed the TGF-beta1-induced protein expression of FN (0.59 +- 0.07 folds, P = 0.008), COL3 (0.48 +- 0.08 folds, P = 0.001), and alpha-SMA (0.61 +- 0.03 folds, P = 0.008) in HPFs.	bromfenac	9-18	fibronectin 1	Homo sapiens	74-76
30908581-9	2019	Conclusions: Bromfenac protects against TGF-beta1-induced synthesis of FN, alpha-SMA, and COL3 in HPFs and HConFs at least in part by inactivating the AKT and ERK pathways.	bromfenac	13-22	transforming growth factor beta 1	Homo sapiens	40-49
30908581-9	2019	Conclusions: Bromfenac protects against TGF-beta1-induced synthesis of FN, alpha-SMA, and COL3 in HPFs and HConFs at least in part by inactivating the AKT and ERK pathways.	bromfenac	13-22	AKT serine/threonine kinase 1	Homo sapiens	151-154
30908581-9	2019	Conclusions: Bromfenac protects against TGF-beta1-induced synthesis of FN, alpha-SMA, and COL3 in HPFs and HConFs at least in part by inactivating the AKT and ERK pathways.	bromfenac	13-22	mitogen-activated protein kinase 1	Homo sapiens	159-162
30296325-9	2018	CONCLUSIONS: A smaller expression of IL-6 to the overall cytokine network value was observed in cases receiving preoperative bromfenac 0.09%, explaining improved maintenance of intraoperative mydriasis.	bromfenac	125-134	interleukin 6	Homo sapiens	37-41
30135178-6	2018	All but two drugs showed substrate affinity to OAT2, whereas four (bromfenac, entacapone, fluorescein, and nateglinide) also showed OATP1B1 activity in transfected cells.	bromfenac	67-76	solute carrier organic anion transporter family member 1B1	Homo sapiens	132-139
27832276-8	2016	In agreement with these data, hypertrophy of astrocytes and Muller cells and expression of glial fibrillary acidic protein and vimentin were greatly diminished by bromfenac treatment.	bromfenac	163-172	vimentin	Rattus norvegicus	127-135
27442130-1	2017	PURPOSE: To evaluate the analgesic effect of bromfenac, a topically administered nonsteroidal antiinflammatory agent, in patients undergoing intravitreal injections (IVIs) of anti-vascular endothelial growth factor agents.	bromfenac	45-54	vascular endothelial growth factor A	Homo sapiens	180-214
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.	bromfenac	73-82	mitochondrially encoded cytochrome c oxidase I	Homo sapiens	134-139
25006692-1	2014	BACKGROUND: According to recent studies, the newest strategy for the treatment of exudative age-related macular degeneration is to combine anti-VEGF agents with non-steroid anti-inflammatory drugs (NSAIDs) such as nepafenac and bromfenac to decrease the frequency of intravitreal injections.	bromfenac	228-237	vascular endothelial growth factor A	Homo sapiens	144-148
24796320-4	2014	FR-190997 stimulated the production of prostaglandins (PGs) in h-CM and h-TM cells (EC50 = 15-19 nM; Emax = 27-33%); an effect that was reduced by the cyclooxygenase-2 inhibitor bromfenac, and by HOE-140.	bromfenac	178-187	prostaglandin G/H synthase 2	Macaca fascicularis	151-167
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.	bromfenac	73-82	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	179-184
24796327-10	2014	CONCLUSIONS: Topical bromfenac can penetrate into the retinochoroidal tissues in high enough concentrations to inhibit COX-2 and exerts its inhibitory effect on the blood-retinal barrier breakdown in an experimental retinochoroidal inflammation in rabbits.	bromfenac	21-30	cytochrome c oxidase subunit II	Oryctolagus cuniculus	119-124
22570544-1	2012	Ophthalmic bromfenac sodium sesquihydrate is a topically applied selective cyclooxygenase (COX)-2 inhibitor.	bromfenac	11-41	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	75-97
19668566-5	2009	The unique chemical structure of bromfenac makes it both a potent inhibitor of the COX-2 enzyme and a highly lipophilic molecule that rapidly penetrates to produce early and sustained drug levels in all ocular tissues.	bromfenac	33-42	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	83-88
21709668-13	2011	The results showed that topical bromfenac led to translocation of Nrf2 and induction of HO-1 in CNV lesions and that the number of infiltrating macrophages at the CNV lesion decreased.	bromfenac	32-41	NFE2 like bZIP transcription factor 2	Rattus norvegicus	66-70
21709668-13	2011	The results showed that topical bromfenac led to translocation of Nrf2 and induction of HO-1 in CNV lesions and that the number of infiltrating macrophages at the CNV lesion decreased.	bromfenac	32-41	heme oxygenase 1	Rattus norvegicus	88-92
21709668-15	2011	VEGF increased in the ocular fluid after laser treatment and was inhibited by bromfenac and SnMP canceling these effects.	bromfenac	78-87	vascular endothelial growth factor A	Rattus norvegicus	0-4
21351868-11	2011	Aqueous and ICB bromfenac levels exceeded its IC(50) for COX-2 at peak and trough, but not for COX-1 at trough aqueous levels and peak and trough ICB levels.	bromfenac	16-25	cytochrome c oxidase subunit II	Oryctolagus cuniculus	57-62