PMID-sentid Pub_year Sent_text compound_name comp_offset prot_official_name organism prot_offset 35083944-0 2022 Diflunisal treatment is associated with improved survival for patients with early stage wild-type transthyretin (ATTR) amyloid cardiomyopathy: the Boston University Amyloidosis Center experience. Diflunisal 0-10 transthyretin Homo sapiens 98-111 34225167-4 2021 Here, we investigated the inhibitory activities of anthraquinone and xanthone derivatives against amyloid aggregation, and found that xanthone-2-carboxylic acid with one chlorine or methyl group has strong inhibitory activity comparable with that of diflunisal, which is one of the best known stabilizers of transthyretin. Diflunisal 250-260 transthyretin Homo sapiens 308-321 34272629-0 2022 The use of diflunisal for transthyretin cardiac amyloidosis: a review. Diflunisal 11-21 transthyretin Homo sapiens 26-39 34272629-2 2022 Diflunisal, an agent that stabilizes TTR, has been used as an off-label therapeutic for ATTR-CM. Diflunisal 0-10 transthyretin Homo sapiens 37-40 34272629-4 2022 We searched the PubMed, MEDLINE, and Embase databases for studies that reported on the use of diflunisal therapy for patients with ATTR-CM. Diflunisal 94-104 transthyretin Homo sapiens 131-135 35083944-0 2022 Diflunisal treatment is associated with improved survival for patients with early stage wild-type transthyretin (ATTR) amyloid cardiomyopathy: the Boston University Amyloidosis Center experience. Diflunisal 0-10 transthyretin Homo sapiens 113-117 35083944-1 2022 BACKGROUND: Diflunisal is a non-steroidal anti-inflammatory drug that stabilises transthyretin (TTR) and reduces neurologic deterioration in patients with polyneuropathy caused by hereditary transthyretin amyloidosis (ATTRv). Diflunisal 12-22 transthyretin Homo sapiens 81-94 35083944-1 2022 BACKGROUND: Diflunisal is a non-steroidal anti-inflammatory drug that stabilises transthyretin (TTR) and reduces neurologic deterioration in patients with polyneuropathy caused by hereditary transthyretin amyloidosis (ATTRv). Diflunisal 12-22 transthyretin Homo sapiens 96-99 35083944-2 2022 METHODS: We conducted a retrospective cohort study of patients with wild-type transthyretin cardiac amyloidosis (ATTRwt-CM) treated with diflunisal for at least one year between 2009 and 2016 at the Boston University Amyloidosis Centre. Diflunisal 137-147 transthyretin Homo sapiens 78-91 34772213-4 2021 Diflunisal stabilizes the transthyretin (TTR) tetramer and prevents the misfolding of monomers and dimers from forming amyloid deposits in the heart. Diflunisal 0-10 transthyretin Homo sapiens 26-39 34772213-4 2021 Diflunisal stabilizes the transthyretin (TTR) tetramer and prevents the misfolding of monomers and dimers from forming amyloid deposits in the heart. Diflunisal 0-10 transthyretin Homo sapiens 41-44 34272629-10 2022 The 2 studies that compared diflunisal versus no treatment found improvements in TTR concentration, left atrial volume index, cardiac troponin I, and global longitudinal strain. Diflunisal 28-38 transthyretin Homo sapiens 81-84 34272629-11 2022 Overall, diflunisal use was associated with decreased mortality and number of orthotopic heart transplant in ATTR-CM patients. Diflunisal 9-19 transthyretin Homo sapiens 109-113 34272629-13 2022 This systematic review supports the use of diflunisal for ATTR-CM. Diflunisal 43-53 transthyretin Homo sapiens 58-62 34491302-9 2022 This has led to the introduction of several first-in-class pharmaceuticals with actions targeted at inhibiting the various phases of amyloidosis: TTR stabilizers include diflunisal and first-in-class, Food and Drug Administration (FDA)-approved tafamidis; TTR silencers include patisiran and inotersen; fibril disrupters include doxycycline with tauroursodeoxycholic acid; and alternative agents include green tea extract and curcumin. Diflunisal 170-180 transthyretin Homo sapiens 146-149 35083944-6 2022 Patients in the diflunisal group were younger (73.8 vs 76.8 years, p = 0.034), with lower B-type natriuretic peptide (BNP, 335 +/- 67 vs. 520 +/- 296 pg/mL, p = 0.006), similar troponin I (0.1 +/- 0.1 vs 0.2 +/- 0.3 ng/mL, p = 0.09), and better renal function (eGFR 67 +/- 17 vs 53 +/- 18 mL/min/1.73m2, p = 0.0002) at baseline. Diflunisal 16-26 natriuretic peptide B Homo sapiens 118-121 35083944-8 2022 Diflunisal administration was associated with improved survival in unadjusted analysis (HR 0.13, 95% CI 0.05 - 0.36, p < 0.001) that persisted after adjustment for age, baseline BNP, eGFR, troponin I, interventricular septal thickness, and left ventricular ejection fraction (HR 0.18, 95% CI 0.06 - 0.51, p = 0.0006). Diflunisal 0-10 natriuretic peptide B Homo sapiens 178-181 35083944-8 2022 Diflunisal administration was associated with improved survival in unadjusted analysis (HR 0.13, 95% CI 0.05 - 0.36, p < 0.001) that persisted after adjustment for age, baseline BNP, eGFR, troponin I, interventricular septal thickness, and left ventricular ejection fraction (HR 0.18, 95% CI 0.06 - 0.51, p = 0.0006). Diflunisal 0-10 epidermal growth factor receptor Homo sapiens 183-187 2498384-6 1989 T4; n = 3; P less than 0.001], while mefenamic acid, diflunisal, and meclofenamic acid were 20-26% as potent as T4 in their interaction with TTR. Diflunisal 53-63 transthyretin Homo sapiens 141-144 32311072-37 2020 Results from placebo-controlled trials indicate that tafamidis, diflunisal, patisiran, and inotersen may be beneficial in TTR-FAP, but further investigations are needed. Diflunisal 64-74 transthyretin Homo sapiens 122-125 4041343-2 1985 During diflunisal treatment, peak plasma concentration of oxazepam significantly decreased from 387 +/- 18 ng ml-1 (mean +/- s.e. Diflunisal 7-17 interleukin 17F Homo sapiens 110-114 6547486-1 1984 Sixteen hyperuricemic gouty patients were treated with diflunisal, a novel salicylate, 500 mg BID. Diflunisal 55-65 BH3 interacting domain death agonist Homo sapiens 94-97 33129740-4 2021 Twelve of those patients concomitantly received diflunisal as a "TTR-stabilizing" drug. Diflunisal 48-58 transthyretin Homo sapiens 65-68 32948978-9 2020 However, as the efficacy of orally administered tafamidis and diflunisal, which stabilize TTR tetramers, was suggested in the early 2010s, such late-onset patients have also become targets for disease-modifying therapies. Diflunisal 62-72 transthyretin Homo sapiens 90-93 32924851-10 2022 Also diflunisal was predicted as potential antischistosomal drug with binding energies of -168.641 +- 20.370 and -290.117 +- 43.800 KJ/mol for sulfotransferase and TGR respectively. Diflunisal 5-15 thioredoxin reductase 3 Homo sapiens 164-167 32924851-11 2022 Non-covalent interactions and conformational changes were responsible for molecular recognitions and specificities and average bond measurement showed that carboxylic functional groups in diflunisal and tolmetin may interact covalently with -SH group of Cys159 in TGR. Diflunisal 188-198 thioredoxin reductase 3 Homo sapiens 264-267 3548984-7 1986 Diflunisal, however, offers a more acceptable BID treatment schedule. Diflunisal 0-10 BH3 interacting domain death agonist Homo sapiens 46-49 4041343-4 1985 In vitro, diflunisal, at concentrations of 125 to 1000 micrograms ml-1, significantly displaced oxazepam from its plasma protein binding, the free fraction of oxazepam increasing by 28 to 56%. Diflunisal 10-20 interleukin 17F Homo sapiens 66-70 359244-6 1978 The slight increase in prothrombin time seen when diflunisal and acenocoumarol were co-administered is not considered to be of major clinical importance. Diflunisal 50-60 coagulation factor II, thrombin Homo sapiens 23-34 33852912-7 2021 Increased ac-tau in human AD brain is further augmented in AD patients with history of TBI, and patients receiving the p300/CBP inhibitors salsalate or diflunisal exhibit decreased incidence of AD and clinically diagnosed TBI. Diflunisal 152-162 microtubule associated protein tau Homo sapiens 13-16 33852912-7 2021 Increased ac-tau in human AD brain is further augmented in AD patients with history of TBI, and patients receiving the p300/CBP inhibitors salsalate or diflunisal exhibit decreased incidence of AD and clinically diagnosed TBI. Diflunisal 152-162 E1A binding protein p300 Homo sapiens 119-123 33852912-7 2021 Increased ac-tau in human AD brain is further augmented in AD patients with history of TBI, and patients receiving the p300/CBP inhibitors salsalate or diflunisal exhibit decreased incidence of AD and clinically diagnosed TBI. Diflunisal 152-162 CREB binding protein Homo sapiens 124-127 32828431-6 2020 Of the derivatives reported here, the best inhibitor of TTR fibrillogenesis, 1d, exhibits an activity similar to diflunisal. Diflunisal 113-123 transthyretin Homo sapiens 56-59 31805416-2 2020 Diflunisal is an approved non-steroidal anti-inflammatory drug (NSAID) that stabilizes TTR, with limited data available regarding effects on cardiac structure and function. Diflunisal 0-10 transthyretin Homo sapiens 87-90 31805416-5 2020 At baseline, patients treated with diflunisal were younger (68 vs 77 y, p=0.0001), with lower B-type natriuretic peptide (BNP, 249 vs 545 pg/ml, p=0.009) and serum creatinine (1.1 vs 1.2 mg/dl, p=0.04), but similar TTR concentration (p=0.31), cardiac troponin I (p=0.06), and GLS (p=0.67). Diflunisal 35-45 natriuretic peptide B Homo sapiens 94-120 31805416-5 2020 At baseline, patients treated with diflunisal were younger (68 vs 77 y, p=0.0001), with lower B-type natriuretic peptide (BNP, 249 vs 545 pg/ml, p=0.009) and serum creatinine (1.1 vs 1.2 mg/dl, p=0.04), but similar TTR concentration (p=0.31), cardiac troponin I (p=0.06), and GLS (p=0.67). Diflunisal 35-45 natriuretic peptide B Homo sapiens 122-125 31805416-5 2020 At baseline, patients treated with diflunisal were younger (68 vs 77 y, p=0.0001), with lower B-type natriuretic peptide (BNP, 249 vs 545 pg/ml, p=0.009) and serum creatinine (1.1 vs 1.2 mg/dl, p=0.04), but similar TTR concentration (p=0.31), cardiac troponin I (p=0.06), and GLS (p=0.67). Diflunisal 35-45 transthyretin Homo sapiens 215-218 31805416-6 2020 At follow-up, diflunisal untreated vs. treated patients showed differences in TTR concentration (19 vs 33 mg/dl, p=0.01) and favorable differences in left atrial volume index (LAVI, +4.6 vs -1.4 ml/m2, p=0.002) and cardiac troponin I (+0.03 vs. -0.01 ng/ml, p=0.01) for the entire cohort. Diflunisal 14-24 transthyretin Homo sapiens 78-81 32445869-9 2020 Then, we identified three FLB analogues (diflunisal, CHF-5074 and HCT1026) forming stable complexes with PD-L1. Diflunisal 41-51 CD274 molecule Homo sapiens 105-110 31473362-6 2019 Distinct interactions with TTR appear to characterize flurbiprofen analogues and the NSAID diflunisal and its analogues as TTR stabilizers. Diflunisal 91-101 transthyretin Homo sapiens 27-30 31473362-6 2019 Distinct interactions with TTR appear to characterize flurbiprofen analogues and the NSAID diflunisal and its analogues as TTR stabilizers. Diflunisal 91-101 transthyretin Homo sapiens 123-126 31548507-4 2019 Indeed, molecular modeling of PLCgamma1 with SLP76 peptide and with previously reported inhibitors (ritonavir, anethole, daunorubicin, diflunisal, and rosiglitazone) facilitated the identification of the common critical residues (Gln805, Arg806, Asp808, Glu809, Asp825, Gly827, and Trp828) as well as the quantification of their interaction through binding energies calculations. Diflunisal 135-145 phospholipase C gamma 1 Homo sapiens 30-39 31418171-3 2019 Here we show that diflunisal, an aspirin-like nonsteroidal anti-inflammatory drug (NSAID) that has been in clinical use for decades, specifically inhibits in vitro and in vivo the chemotactic activity of HMGB1 at nanomolar concentrations, at least in part by binding directly to both HMGB1 and CXCL12 and disrupting their heterocomplex. Diflunisal 18-28 high mobility group box 1 Homo sapiens 204-209 31418171-3 2019 Here we show that diflunisal, an aspirin-like nonsteroidal anti-inflammatory drug (NSAID) that has been in clinical use for decades, specifically inhibits in vitro and in vivo the chemotactic activity of HMGB1 at nanomolar concentrations, at least in part by binding directly to both HMGB1 and CXCL12 and disrupting their heterocomplex. Diflunisal 18-28 high mobility group box 1 Homo sapiens 284-289 31418171-3 2019 Here we show that diflunisal, an aspirin-like nonsteroidal anti-inflammatory drug (NSAID) that has been in clinical use for decades, specifically inhibits in vitro and in vivo the chemotactic activity of HMGB1 at nanomolar concentrations, at least in part by binding directly to both HMGB1 and CXCL12 and disrupting their heterocomplex. Diflunisal 18-28 C-X-C motif chemokine ligand 12 Homo sapiens 294-300 31548507-4 2019 Indeed, molecular modeling of PLCgamma1 with SLP76 peptide and with previously reported inhibitors (ritonavir, anethole, daunorubicin, diflunisal, and rosiglitazone) facilitated the identification of the common critical residues (Gln805, Arg806, Asp808, Glu809, Asp825, Gly827, and Trp828) as well as the quantification of their interaction through binding energies calculations. Diflunisal 135-145 lymphocyte cytosolic protein 2 Homo sapiens 45-50 30720135-5 2019 The present authors proposed that aspirin, diaspirin and analogues, and diflunisal (a salicylic acid derivative) may rapidly perturb EGF and EGF receptor (EGFR) internalisation. Diflunisal 72-82 epidermal growth factor Homo sapiens 133-136 30720135-5 2019 The present authors proposed that aspirin, diaspirin and analogues, and diflunisal (a salicylic acid derivative) may rapidly perturb EGF and EGF receptor (EGFR) internalisation. Diflunisal 72-82 epidermal growth factor receptor Homo sapiens 141-153 30720135-5 2019 The present authors proposed that aspirin, diaspirin and analogues, and diflunisal (a salicylic acid derivative) may rapidly perturb EGF and EGF receptor (EGFR) internalisation. Diflunisal 72-82 epidermal growth factor receptor Homo sapiens 155-159 30466940-2 2019 In this work, a complex between iron(II) and diflunisal was prepared in the solid state, exhibiting the following composition: [Fe(diflunisal)2(H2O)2], (Fe(dif)2). Diflunisal 45-55 immediate early response 3 Homo sapiens 153-161 30688456-5 2019 In addition, 4 synergistically increased the stabilization activity of diflunisal, one of the most potent TTR amyloidogenesis inhibitors. Diflunisal 71-81 transthyretin Homo sapiens 106-109 29663481-6 2018 Similarly, pharmacological activation of AMPK by treatment with diflunisal, A769662, and ZLN024 reduced the expression of v-ATPase subunits and profibrogenic markers. Diflunisal 64-74 protein kinase AMP-activated catalytic subunit alpha 1 Homo sapiens 41-45 30388377-2 2018 Diflunisal, a nonsteroidal anti-inflammatory drug (NSAID), has demonstrated transthyretin stabilization in vitro and slowing of polyneuropathy progression in the hereditary ATTR subtype (ATTRm). Diflunisal 0-10 transthyretin Homo sapiens 173-177 30388377-3 2018 However, the use of diflunisal has only been described in a small cohort of patients with ATTR cardiac amyloidosis (CA). Diflunisal 20-30 transthyretin Homo sapiens 90-94 30388377-4 2018 We hypothesized that selected patients with ATTR-CA, both hereditary and wild-type (ATTRwt), would tolerate diflunisal with limited adverse events. Diflunisal 108-118 transthyretin Homo sapiens 44-48 30388377-5 2018 MATERIALS AND METHODS: This is a retrospective, longitudinal study of 23 patients with ATTR-CA (10 ATTRm and 13 ATTRwt) diagnosed at the Cleveland Clinic from May 2007 to August 2017 who were treated with diflunisal. Diflunisal 205-215 transthyretin Homo sapiens 87-91 30388377-16 2018 Diflunisal can be safely used in a selected group of ATTR-CA patients with appropriate clinical, renal and hematologic monitoring. Diflunisal 0-10 transthyretin Homo sapiens 53-57 29663481-6 2018 Similarly, pharmacological activation of AMPK by treatment with diflunisal, A769662, and ZLN024 reduced the expression of v-ATPase subunits and profibrogenic markers. Diflunisal 64-74 ATPase, H+ transporting, lysosomal V0 subunit D2 Mus musculus 122-130 29330472-3 2018 Thus, the TTR stabilizers, such as Tafamidis and Diflunisal, are now in clinical trials. Diflunisal 49-59 transthyretin Mus musculus 10-13 29941560-12 2018 Our studies of a unique duplication mutation explain its diflunisal-resistant nature, identify misfolding pathways for amyloidogenic TTR variants, and provide therapeutic targets to inhibit amyloid fibril formation by variant TTR. Diflunisal 57-67 transthyretin Homo sapiens 133-136 29941560-12 2018 Our studies of a unique duplication mutation explain its diflunisal-resistant nature, identify misfolding pathways for amyloidogenic TTR variants, and provide therapeutic targets to inhibit amyloid fibril formation by variant TTR. Diflunisal 57-67 transthyretin Homo sapiens 226-229 28817613-7 2017 We conclude that diflunisal affects the cell membrane organization and inhibits prestin-associated charge transfer and electromotility at physiological chloride concentrations. Diflunisal 17-27 solute carrier family 26, member 5 Mus musculus 80-87 29449366-9 2018 Further, TTR values at 1- and 2-year follow-ups were significantly lower (P<0.001) in untreated patients (n=23) compared with those treated with TTR stabilizer, diflunisal (n=12), after baseline evaluation. Diflunisal 164-174 transthyretin Homo sapiens 9-12 29449366-10 2018 During 2-year follow-up, unchanged TTR corresponded to increased cTn-I (P=0.006) in untreated patients; conversely, the diflunisal-treated group showed increased TTR (P=0.001) and stabilized cTn-I and left ventricular ejection fraction at 1 year. Diflunisal 120-130 transthyretin Homo sapiens 162-165 29449366-10 2018 During 2-year follow-up, unchanged TTR corresponded to increased cTn-I (P=0.006) in untreated patients; conversely, the diflunisal-treated group showed increased TTR (P=0.001) and stabilized cTn-I and left ventricular ejection fraction at 1 year. Diflunisal 120-130 troponin I3, cardiac type Homo sapiens 191-196 28771355-3 2017 For proof-of-principle, the clinically relevant glucagon-like peptide 1 (GLP-1) was functionalized with diflunisal, indomethacin, or both. Diflunisal 104-114 glucagon Mus musculus 48-71 28771355-3 2017 For proof-of-principle, the clinically relevant glucagon-like peptide 1 (GLP-1) was functionalized with diflunisal, indomethacin, or both. Diflunisal 104-114 glucagon Mus musculus 73-78 28817613-0 2017 Diflunisal inhibits prestin by chloride-dependent mechanism. Diflunisal 0-10 solute carrier family 26, member 5 Mus musculus 20-27 28817613-5 2017 We monitored the impact of diflunisal on the prestin-dependent non-linear capacitance and electromotility. Diflunisal 27-37 solute carrier family 26, member 5 Mus musculus 45-52 28817613-6 2017 We found that diflunisal triggers two prestin-associated effects: a chloride independent increase in the surface area and the specific capacitance of the membrane, and a chloride dependent inhibition of the charge transfer and the electromotility in outer hair cells. Diflunisal 14-24 solute carrier family 26, member 5 Mus musculus 38-45 28775266-6 2017 We identified six novel molecules, including 2 approved drugs, diflusinal and loperamide, with Kd values in the low micromolar range, that block the human ClC-Kb channel and that could be used as starting point to design novel chemical probes for this potential therapeutic target. Diflunisal 63-73 chloride voltage-gated channel Kb Homo sapiens 155-161 28111409-4 2017 The patient started taking diflunisal as a stabilizer which is one of the advanced therapies for ATTR, and then the heart failure symptoms and brain natriuretic peptide (BNP) level improved in short-term follow-up. Diflunisal 27-37 transthyretin Homo sapiens 97-101 28111409-4 2017 The patient started taking diflunisal as a stabilizer which is one of the advanced therapies for ATTR, and then the heart failure symptoms and brain natriuretic peptide (BNP) level improved in short-term follow-up. Diflunisal 27-37 natriuretic peptide B Homo sapiens 143-168 28111409-4 2017 The patient started taking diflunisal as a stabilizer which is one of the advanced therapies for ATTR, and then the heart failure symptoms and brain natriuretic peptide (BNP) level improved in short-term follow-up. Diflunisal 27-37 natriuretic peptide B Homo sapiens 170-173 27244239-0 2016 Salicylate, diflunisal and their metabolites inhibit CBP/p300 and exhibit anticancer activity. Diflunisal 12-22 CREB binding protein Homo sapiens 53-61 27497715-10 2016 Pharmacologic agents, including diflunisal, tafamidis, small interfering ribonucleic acid, and doxycycline, have shown promising activity in stabilizing TTR from misfolding into fibrils and are being actively investigated. Diflunisal 32-42 transthyretin Homo sapiens 153-156 27244239-5 2016 We used a chemical structure-similarity search to identify another anti-inflammatory drug, diflunisal, that inhibits p300 more potently than salicylate. Diflunisal 91-101 E1A binding protein p300 Homo sapiens 117-121 27244239-7 2016 Finally, we found that diflunisal suppressed the growth of p300-dependent leukemia cell lines expressing AML1-ETO fusion protein in vitro and in vivo. Diflunisal 23-33 E1A binding protein p300 Homo sapiens 59-63 27244239-7 2016 Finally, we found that diflunisal suppressed the growth of p300-dependent leukemia cell lines expressing AML1-ETO fusion protein in vitro and in vivo. Diflunisal 23-33 RUNX family transcription factor 1 Homo sapiens 105-109 27244239-7 2016 Finally, we found that diflunisal suppressed the growth of p300-dependent leukemia cell lines expressing AML1-ETO fusion protein in vitro and in vivo. Diflunisal 23-33 RUNX1 partner transcriptional co-repressor 1 Homo sapiens 110-113 26800456-7 2016 EXPERT OPINION: Due to the data on efficacy, tolerability, safety, tafamidis and diflunisal became the first line anti-amyloid treatment in stage 1 TTR-FAP. Diflunisal 81-91 transthyretin Homo sapiens 148-151 25946000-10 2015 Among the 9 drugs, 4 drugs (diflunisal, nabumetone, niflumic acid and valdecoxib) targeting COX2 (prostaglandin G/H synthase 2) were repurposed for treating type 1 diabetes, and 2 drugs (phenoxybenzamine and idazoxan) targeting ADRA2A (Alpha-2A adrenergic receptor) had a new indication for treating type 2 diabetes. Diflunisal 28-38 mitochondrially encoded cytochrome c oxidase II Homo sapiens 92-96 25819286-8 2015 The patient is being treated with diflunisal, an oral TTR stabilising agent. Diflunisal 34-44 transthyretin Homo sapiens 54-57 25946000-10 2015 Among the 9 drugs, 4 drugs (diflunisal, nabumetone, niflumic acid and valdecoxib) targeting COX2 (prostaglandin G/H synthase 2) were repurposed for treating type 1 diabetes, and 2 drugs (phenoxybenzamine and idazoxan) targeting ADRA2A (Alpha-2A adrenergic receptor) had a new indication for treating type 2 diabetes. Diflunisal 28-38 prostaglandin-endoperoxide synthase 2 Homo sapiens 98-126 25522350-6 2015 Diflunisal inhibited the UGT1A1 (IC50 = 33.0 mum) and UGT1A9 (IC50 = 19.4 mum). Diflunisal 0-10 UDP glucuronosyltransferase family 1 member A1 Homo sapiens 25-31 25522350-6 2015 Diflunisal inhibited the UGT1A1 (IC50 = 33.0 mum) and UGT1A9 (IC50 = 19.4 mum). Diflunisal 0-10 UDP glucuronosyltransferase family 1 member A9 Homo sapiens 54-60 23416065-1 2013 The cyclooxygenase-2 inhibitor, diflunisal, is used in the clinic for its anti-inflammatory activity. Diflunisal 32-42 prostaglandin-endoperoxide synthase 2 Homo sapiens 4-20 25728271-6 2015 Although the binding affinities of CHF5074 and diflunisal with TTRMet30 were similar, CHF5074 bound TTRVal30 more strongly than did diflunisal, suggesting the potent TTR-stabilizing activity of CHF5074. Diflunisal 47-57 transthyretin Mus musculus 63-66 25394203-3 2015 From a selected set of 77 noniodinated and 77 iodinated diflunisal analogues, a subset of good transthyretin amyloid inhibitors has been obtained with improved turbidimetry inhibition constants, high binding affinity to transthyretin, and good selectivity for TTR compared to other thyroxine binding proteins. Diflunisal 56-66 transthyretin Homo sapiens 95-108 25060417-10 2014 CONCLUSION: Diflunisal might be effective especially for autonomic dysfunction in late-onset FAP with a TTR Val30Met mutation. Diflunisal 12-22 transthyretin Homo sapiens 104-107 24147937-4 2013 Analysis of the halogenated derivatives of two well-known TTR inhibitors has shown that while flufenamic acid affinity for TTR was unchanged by halogenation, diflunisal gradually improves binding up to 1 order of magnitude after iodination through interactions that can be interpreted as a suboptimal XB (carbonyl Thr106: I...O distance 3.96-4.05 A; C-I...O angle 152-156 ) or as rather optimized van der Waals contacts or as a mixture of both. Diflunisal 158-168 transthyretin Homo sapiens 58-61 25478940-12 2015 The interactions of CLU with monomeric and aggregated TTR proceed in a cooperative manner in the presence of diflunisal, a small molecule drug used to stabilize TTR tetramers. Diflunisal 109-119 clusterin Homo sapiens 20-23 25478940-12 2015 The interactions of CLU with monomeric and aggregated TTR proceed in a cooperative manner in the presence of diflunisal, a small molecule drug used to stabilize TTR tetramers. Diflunisal 109-119 transthyretin Homo sapiens 54-57 25478940-12 2015 The interactions of CLU with monomeric and aggregated TTR proceed in a cooperative manner in the presence of diflunisal, a small molecule drug used to stabilize TTR tetramers. Diflunisal 109-119 transthyretin Homo sapiens 161-164 26611723-6 2015 The TTR stabilizers tafamidis and diflunisal slow disease progression in some patients with ATTR amyloidosis with polyneuropathy, and the postulated synergistic effect of doxycycline and tauroursodeoxycholic acid on dissolution of amyloid is under investigation. Diflunisal 34-44 transthyretin Homo sapiens 92-96 25672679-7 2014 Recently, the clinical effects of TTR tetramer stabilizers, tafamidis and diflunisal, were demonstrated in randomised clinical trials, and tafamidis has been approved for the treatment of hereditary ATTR amyloidosis in European countries and in Japan. Diflunisal 74-84 transthyretin Homo sapiens 34-37 23416065-2 2013 About 99% of a dose of diflunisal is unavailable for reaction with the target enzyme, because diflunisal strongly binds to human serum albumin (HSA). Diflunisal 23-33 albumin Homo sapiens 129-142 23416065-2 2013 About 99% of a dose of diflunisal is unavailable for reaction with the target enzyme, because diflunisal strongly binds to human serum albumin (HSA). Diflunisal 94-104 albumin Homo sapiens 129-142 21865539-8 2011 Several of these ligands stabilized TTR in human serum more effectively than diflunisal, which is a well-studied inhibitor of TTR aggregation, and may be promising leads for the treatment or prevention of TTR-mediated cardiomyopathy. Diflunisal 77-87 transthyretin Homo sapiens 126-129 23628406-2 2013 The solubility of NSAIDs (Ketoprofen, Ibuprofen and Diflunisal) was investigated in the presence of PPO@PAMAM dendrimers at room temperature in buffer solution. Diflunisal 52-62 protoporphyrinogen oxidase Homo sapiens 100-109 22733274-6 2012 Among them, eight, namely Atorvastatin, Bumetanide, Candesartan, Carbidopa, Diclofenac, Diflunisal, Eprosartan, and Sulindac, were identified as potential inhibitors of LEDGF/p75- HIV-1 IN interaction, whose IC(50) values ranged from 6.5 muM to 36.8 muM. Diflunisal 88-98 PC4 and SFRS1 interacting protein 1 Homo sapiens 169-178 22747647-0 2012 Diflunisal for ATTR cardiac amyloidosis. Diflunisal 0-10 transthyretin Homo sapiens 15-19 22747647-3 2012 Diflunisal, a nonsteroidal anti-inflammatory drug, can stabilize the TTR tetramer in vitro and may prevent misfolding monomers and dimers from forming amyloid deposits in the heart. Diflunisal 0-10 transthyretin Homo sapiens 69-72 22747647-5 2012 The authors conducted a single-arm, open-label investigation with a mean follow-up of 0.9 +- 0.3 years to determine the safety and efficacy of diflunisal administration in a cohort of 13 patients with confirmed wild-type or mutant TTR cardiac amyloidosis. Diflunisal 143-153 transthyretin Homo sapiens 231-234 22071090-8 2011 Diflunisal and its complexes exhibit good binding propensity to human or bovine serum albumin protein showing relatively high binding constant values. Diflunisal 0-10 albumin Homo sapiens 80-93 21865539-8 2011 Several of these ligands stabilized TTR in human serum more effectively than diflunisal, which is a well-studied inhibitor of TTR aggregation, and may be promising leads for the treatment or prevention of TTR-mediated cardiomyopathy. Diflunisal 77-87 transthyretin Homo sapiens 126-129 19621084-5 2009 Based on an in vitro fibril formation assay, five of these compounds showed significant inhibition of TTR amyloidogenesis, with two fluorenyl compounds displaying inhibitor efficacy comparable to the well-known TTR inhibitor diflunisal. Diflunisal 225-235 transthyretin Homo sapiens 211-214 17028027-0 2006 Diflunisal stabilizes familial amyloid polyneuropathy-associated transthyretin variant tetramers in serum against dissociation required for amyloidogenesis. Diflunisal 0-10 transthyretin Homo sapiens 65-78 19125186-6 2009 The new TTR fibrillogenesis inhibitors are based on the diflunisal core structure because diflunisal is a registered salicylate drug with NSAID activity now undergoing clinical trials for TTR amyloid diseases. Diflunisal 56-66 transthyretin Homo sapiens 8-11 19125186-6 2009 The new TTR fibrillogenesis inhibitors are based on the diflunisal core structure because diflunisal is a registered salicylate drug with NSAID activity now undergoing clinical trials for TTR amyloid diseases. Diflunisal 56-66 transthyretin Homo sapiens 188-191 19125186-6 2009 The new TTR fibrillogenesis inhibitors are based on the diflunisal core structure because diflunisal is a registered salicylate drug with NSAID activity now undergoing clinical trials for TTR amyloid diseases. Diflunisal 90-100 transthyretin Homo sapiens 8-11 19125186-6 2009 The new TTR fibrillogenesis inhibitors are based on the diflunisal core structure because diflunisal is a registered salicylate drug with NSAID activity now undergoing clinical trials for TTR amyloid diseases. Diflunisal 90-100 transthyretin Homo sapiens 188-191 17107884-0 2006 Orally administered diflunisal stabilizes transthyretin against dissociation required for amyloidogenesis. Diflunisal 20-30 transthyretin Homo sapiens 42-55 17107884-3 2006 Diflunisal binding to the 99% unoccupied L-thyroxine binding sites in TTR also increases the tetramer dissociation barrier; hence, we investigated the feasibility of using diflunisal for the treatment of human TTR amyloidosis using healthy volunteers. Diflunisal 0-10 transthyretin Homo sapiens 70-73 17107884-3 2006 Diflunisal binding to the 99% unoccupied L-thyroxine binding sites in TTR also increases the tetramer dissociation barrier; hence, we investigated the feasibility of using diflunisal for the treatment of human TTR amyloidosis using healthy volunteers. Diflunisal 0-10 transthyretin Homo sapiens 210-213 17107884-6 2006 RESULTS: In the 250 mg bid group, 12 h after the 13th oral dose, the diflunisal serum concentration of 146 +/- 39 microM was sufficient to afford a TTR binding stoichiometry exceeding 0.95 +/- 0.13 ( approximately 1.75 corrected). Diflunisal 69-79 transthyretin Homo sapiens 148-151 17107884-7 2006 Diflunisal binding to TTR at this dose slowed urea-mediated dissociation and acid-mediated TTR aggregation at least, threefold (p < 0.05) in serum and in vitro, consistent with kinetic stabilization of TTR. Diflunisal 0-10 transthyretin Homo sapiens 22-25 17107884-7 2006 Diflunisal binding to TTR at this dose slowed urea-mediated dissociation and acid-mediated TTR aggregation at least, threefold (p < 0.05) in serum and in vitro, consistent with kinetic stabilization of TTR. Diflunisal 0-10 transthyretin Homo sapiens 91-94 17107884-7 2006 Diflunisal binding to TTR at this dose slowed urea-mediated dissociation and acid-mediated TTR aggregation at least, threefold (p < 0.05) in serum and in vitro, consistent with kinetic stabilization of TTR. Diflunisal 0-10 transthyretin Homo sapiens 91-94 17107884-8 2006 CONCLUSION: Diflunisal-mediated kinetic stabilization of TTR should ameliorate TTR amyloidoses, provided that the nonsteroidal anti-inflammatory drug liabilities can be managed clinically. Diflunisal 12-22 transthyretin Homo sapiens 57-60 17107884-8 2006 CONCLUSION: Diflunisal-mediated kinetic stabilization of TTR should ameliorate TTR amyloidoses, provided that the nonsteroidal anti-inflammatory drug liabilities can be managed clinically. Diflunisal 12-22 transthyretin Homo sapiens 79-82 17701470-6 2007 Intraperitoneal administration of diflunisal, a non-steroidal anti-inflammatory drug that binds to TTR in its T4-binding site and inhibits fibril formation in vitro, to human L55P TTR transgenic animals in which the murine TTR gene had been silenced, also stabilizes the circulating mutant protein to in vitro urea denaturation. Diflunisal 34-44 transthyretin Homo sapiens 99-102 17701470-6 2007 Intraperitoneal administration of diflunisal, a non-steroidal anti-inflammatory drug that binds to TTR in its T4-binding site and inhibits fibril formation in vitro, to human L55P TTR transgenic animals in which the murine TTR gene had been silenced, also stabilizes the circulating mutant protein to in vitro urea denaturation. Diflunisal 34-44 transthyretin Mus musculus 180-183 17701470-6 2007 Intraperitoneal administration of diflunisal, a non-steroidal anti-inflammatory drug that binds to TTR in its T4-binding site and inhibits fibril formation in vitro, to human L55P TTR transgenic animals in which the murine TTR gene had been silenced, also stabilizes the circulating mutant protein to in vitro urea denaturation. Diflunisal 34-44 transthyretin Mus musculus 180-183 17028027-6 2006 We also demonstrated that therapeutic serum concentrations of diflunisal (100-200 microM) stabilized serum variant TTR tetramer better than those of flufenamic acid (35-70 microM). Diflunisal 62-72 transthyretin Homo sapiens 115-118 17028027-8 2006 Importantly, diflunisal increased serum TTR stability in FAP patients beyond the level of normal controls. Diflunisal 13-23 transthyretin Homo sapiens 40-43 15080795-0 2004 Selective binding to transthyretin and tetramer stabilization in serum from patients with familial amyloidotic polyneuropathy by an iodinated diflunisal derivative. Diflunisal 142-152 transthyretin Homo sapiens 21-34 15689188-4 2005 In the present paper, the crystal structure of transthyretin complexed with this diflunisal derivative is reported, which enables a detailed analysis of the protein-ligand interactions. Diflunisal 81-91 transthyretin Homo sapiens 47-60 17132209-1 2006 The competitive binding of diflunisal and three well-known uraemic toxins (3-indoxyl sulfate, indole-3-acetic acid and hippuric acid) to bovine serum albumin (BSA), human serum albumin (HSA) and human plasma was studied by direct potentiometry. Diflunisal 27-37 albumin Homo sapiens 144-157 17132209-1 2006 The competitive binding of diflunisal and three well-known uraemic toxins (3-indoxyl sulfate, indole-3-acetic acid and hippuric acid) to bovine serum albumin (BSA), human serum albumin (HSA) and human plasma was studied by direct potentiometry. Diflunisal 27-37 albumin Homo sapiens 171-190 17132209-5 2006 Although diflunisal exhibits high binding affinity for site I of HSA and the three uraemic toxins bind primarily to site II, strong interaction was observed between the drug and the three toxins, which were found to affect the binding of diflunisal on its primary class of binding sites on both BSA and HSA molecules and on human plasma. Diflunisal 9-19 albumin Homo sapiens 65-68 17132209-5 2006 Although diflunisal exhibits high binding affinity for site I of HSA and the three uraemic toxins bind primarily to site II, strong interaction was observed between the drug and the three toxins, which were found to affect the binding of diflunisal on its primary class of binding sites on both BSA and HSA molecules and on human plasma. Diflunisal 9-19 albumin Homo sapiens 303-306 17132209-5 2006 Although diflunisal exhibits high binding affinity for site I of HSA and the three uraemic toxins bind primarily to site II, strong interaction was observed between the drug and the three toxins, which were found to affect the binding of diflunisal on its primary class of binding sites on both BSA and HSA molecules and on human plasma. Diflunisal 238-248 albumin Homo sapiens 65-68 17132209-5 2006 Although diflunisal exhibits high binding affinity for site I of HSA and the three uraemic toxins bind primarily to site II, strong interaction was observed between the drug and the three toxins, which were found to affect the binding of diflunisal on its primary class of binding sites on both BSA and HSA molecules and on human plasma. Diflunisal 238-248 albumin Homo sapiens 303-306 16266291-9 2005 Based on the proposed mechanism for TTR amyloid fibril formation we discuss the action of some of the proposed TTR stabilizers such as derivatives of some NSAIDs (diflunisal, diclofenac, flufenamic acid, and derivatives) and the action of amyloid disrupters such as 4"-iodo-4"-deoxydoxorubicin (I-DOX) and tetracyclines. Diflunisal 163-173 transthyretin Homo sapiens 36-39 16266291-9 2005 Based on the proposed mechanism for TTR amyloid fibril formation we discuss the action of some of the proposed TTR stabilizers such as derivatives of some NSAIDs (diflunisal, diclofenac, flufenamic acid, and derivatives) and the action of amyloid disrupters such as 4"-iodo-4"-deoxydoxorubicin (I-DOX) and tetracyclines. Diflunisal 163-173 transthyretin Homo sapiens 111-114 15210837-7 2004 However, several compounds displayed beta2/3 subunit selectivity, notably loreclezole, R(-)-etomidate, and a group of anti-inflammatory agents including mefenamic acid, flufenamic acid, meclofenamic acid, tolfenamic acid, niflumic acid, and diflunisal. Diflunisal 241-251 potassium calcium-activated channel subfamily M regulatory beta subunit 2 Homo sapiens 37-44 15210837-9 2004 Diflunisal was the most efficacious compound, eliciting greater potentiation than loreclezole (90 +/- 14% and 109 +/- 14% at beta3 and beta2, respectively, compared with 62 +/- 6% and 56 +/- 3%), whereas niflumic acid exhibited the lowest efficacy. Diflunisal 0-10 eukaryotic translation elongation factor 1 beta 2 pseudogene 2 Homo sapiens 125-130 15210837-9 2004 Diflunisal was the most efficacious compound, eliciting greater potentiation than loreclezole (90 +/- 14% and 109 +/- 14% at beta3 and beta2, respectively, compared with 62 +/- 6% and 56 +/- 3%), whereas niflumic acid exhibited the lowest efficacy. Diflunisal 0-10 potassium calcium-activated channel subfamily M regulatory beta subunit 2 Homo sapiens 135-140 15080795-4 2004 Several small compounds, such as diclofenac, diflunisal and flufenamic acid, have been reported to bind to TTR in vitro, in the T4 (thyroxine) binding channel that runs through the TTR tetramer, and consequently are considered to stabilize TTR. Diflunisal 45-55 transthyretin Homo sapiens 107-110 15080795-4 2004 Several small compounds, such as diclofenac, diflunisal and flufenamic acid, have been reported to bind to TTR in vitro, in the T4 (thyroxine) binding channel that runs through the TTR tetramer, and consequently are considered to stabilize TTR. Diflunisal 45-55 transthyretin Homo sapiens 181-184 15080795-4 2004 Several small compounds, such as diclofenac, diflunisal and flufenamic acid, have been reported to bind to TTR in vitro, in the T4 (thyroxine) binding channel that runs through the TTR tetramer, and consequently are considered to stabilize TTR. Diflunisal 45-55 transthyretin Homo sapiens 181-184 15080795-7 2004 We found two diflunisal derivatives that, in contrast with diclofenac, flufenamic acid and diflunisal, displaced T4 from TTR in plasma preferentially over binding to albumin and thyroxine binding globulin. Diflunisal 13-23 transthyretin Homo sapiens 121-124 15080795-7 2004 We found two diflunisal derivatives that, in contrast with diclofenac, flufenamic acid and diflunisal, displaced T4 from TTR in plasma preferentially over binding to albumin and thyroxine binding globulin. Diflunisal 91-101 transthyretin Homo sapiens 121-124 15080795-8 2004 The same diflunisal derivatives also had a stabilizing effect on TTR tetramers in plasma, as studied by isoelectric focusing of whole plasma under semi-denaturing conditions. Diflunisal 9-19 transthyretin Homo sapiens 65-68 15080795-9 2004 In addition, by transmission electron microscopy, we demonstrated that, in contrast with other proposed TTR stabilizers (namely diclofenac, flufenamic acid and diflunisal), one of the diflunisal derivatives tested efficiently inhibited TTR aggregation. Diflunisal 184-194 transthyretin Homo sapiens 236-239 15080795-10 2004 Taken together, our ex vivo and in vitro studies present evidence for the selectivity and efficiency of novel diflunisal derivates as TTR stabilizers and as inhibitors of fibril formation. Diflunisal 110-120 transthyretin Homo sapiens 134-137 14968122-8 2004 The most common familial TTR variants were stabilized substantially by flufenamic acid and inhibitor 1, and to a lesser extent by diflunisal, against acid-mediated fibril formation and chaotrope denaturation, suggesting that this chemotherapeutic option is viable for patients with familial transthyretin amyloidosis. Diflunisal 130-140 transthyretin Homo sapiens 25-28 8737748-9 1996 Diflunisal and nimesulide were > 4-fold selective for PGHS-2, and NS-398 was > 30-fold selective for PGHS-2. Diflunisal 0-10 prostaglandin-endoperoxide synthase 2 Homo sapiens 57-63 11673972-0 2001 Rational design of diflunisal analogues with reduced affinity for human serum albumin. Diflunisal 19-29 albumin Homo sapiens 72-85 10497143-8 1999 UGT1A8, but not UGT1A10, catalyzed the glucuronidation of opioids, bile acids, fatty acids, retinoids, and clinically useful drugs, such as ciprofibrate, furosemide, and diflunisal. Diflunisal 170-180 UDP glucuronosyltransferase family 1 member A8 Homo sapiens 0-6 10463815-4 1999 ALP cleaves phosphate from diflunisal phosphate (DIFP) to produce diflunisal (DIF). Diflunisal 27-37 alkaline phosphatase, placental Homo sapiens 0-3 10463815-4 1999 ALP cleaves phosphate from diflunisal phosphate (DIFP) to produce diflunisal (DIF). Diflunisal 49-52 alkaline phosphatase, placental Homo sapiens 0-3 14711308-0 2004 Diflunisal analogues stabilize the native state of transthyretin. Diflunisal 0-10 transthyretin Homo sapiens 51-64 14711308-2 2004 Analogues of diflunisal, an FDA-approved nonsteroidal antiinflammatory drug (NSAID), were synthesized and evaluated as inhibitors of transthyretin (TTR) aggregation, including amyloid fibril formation. Diflunisal 13-23 transthyretin Homo sapiens 133-146 14711308-2 2004 Analogues of diflunisal, an FDA-approved nonsteroidal antiinflammatory drug (NSAID), were synthesized and evaluated as inhibitors of transthyretin (TTR) aggregation, including amyloid fibril formation. Diflunisal 13-23 transthyretin Homo sapiens 148-151 10991954-5 2000 Diflunisal, ketoprofen, flurbiprofen, indomethacin, naproxen, and ibuprofen were equally or more effective (IC(50) = 0.85-8 microM) than probenecid or betamipron, two known potent inhibitors of hOAT1 (IC(50) = 8 and 6 microM, respectively) with in vivo nephroprotective effects. Diflunisal 0-10 solute carrier family 22 member 6 Homo sapiens 194-199 9714294-7 1998 Diflunisal, 2-hydroxydodecanoic acid, and nalidixic acid inhibited the medium chain acyl-CoA synthetase activity for hexanoic acid, with Ki values of 0.8, 4.4, and 12.3 microM, respectively. Diflunisal 0-10 acyl-CoA synthetase medium chain family member 1 Homo sapiens 71-103 9180355-0 1997 Conjugation-deconjugation cycling of diflunisal via beta-glucuronidase catalyzed hydrolysis of its acyl glucuronide in the rat. Diflunisal 37-47 glucuronidase, beta Rattus norvegicus 52-70 9180355-2 1997 The metabolic disposition kinetics of diflunisal, a compound undergoing transformation to an acyl and phenyl glucuronide, were studied in rats under control conditions and following administration of D-glucaro-1,4-lactone, a potent and specific beta-glucuronidase inhibitor. Diflunisal 38-48 glucuronidase, beta Rattus norvegicus 245-263 8216368-0 1993 Studies on the reactivity of acyl glucuronides--V. Glucuronide-derived covalent binding of diflunisal to bladder tissue of rats and its modulation by urinary pH and beta-glucuronidase. Diflunisal 91-101 glucuronidase, beta Rattus norvegicus 165-183 8867997-14 1996 These results demonstrate that the in vitro glucuronidation rate of diflunisal may be affected by the microsomal beta-glucuronidase activity particularly when using rat liver microsomes. Diflunisal 68-78 glucuronidase, beta Rattus norvegicus 113-131 8867997-15 1996 Our results also demonstrate that the human kidney has an important UGT-activity towards diflunisal. Diflunisal 89-99 UDP glucuronosyltransferase family 1 member A complex locus Homo sapiens 68-71 8743402-2 1996 The UDP-glucuronosyltransferase (UGT) activity was determined toward the following substrates: 4-nitrophenol, propofol, (-)-morphine (formation of the 3-glucuronide), and diflunisal (formation of the phenolic and acyl glucuronides). Diflunisal 171-181 UDP glucuronosyltransferase family 1 member A complex locus Homo sapiens 4-31 8743402-2 1996 The UDP-glucuronosyltransferase (UGT) activity was determined toward the following substrates: 4-nitrophenol, propofol, (-)-morphine (formation of the 3-glucuronide), and diflunisal (formation of the phenolic and acyl glucuronides). Diflunisal 171-181 UDP glucuronosyltransferase family 1 member A complex locus Homo sapiens 33-36 7768255-8 1995 This was the result of a significant decrease in the plasma clearance of diflunisal from 5.8 (control) to 3.4 ml.min-1 (probenecid co-administration). Diflunisal 73-83 CD59 molecule (CD59 blood group) Homo sapiens 113-118 7691442-3 1993 The activity of ALP is measured with the substrate diflunisal phosphate; the released diflunisal forms highly fluorescent complexes with Tb(3+)-EDTA that are quantified with microsecond time-resolved fluorometry. Diflunisal 51-61 alkaline phosphatase, placental Homo sapiens 16-19 1606992-2 1992 The plasma clearance of total (bound + unbound) diflunisal was 10.2 ml.min-1 in the control subjects and it was not affected by cirrhosis (10.9 ml.min-1). Diflunisal 48-58 CD59 molecule (CD59 blood group) Homo sapiens 71-76 8290710-1 1993 This report describes a patient who developed acute rhabdomyolysis and acute renal failure following the application of MAST trousers associated with an overdose of diflunisal. Diflunisal 165-175 SPG21 abhydrolase domain containing, maspardin Homo sapiens 120-124 1606992-4 1992 Plasma clearance of unbound diflunisal was significantly impaired in cirrhosis: 11.5 l.min-1 in control subjects vs 7.41.min-1 in cirrhotics. Diflunisal 28-38 CD59 molecule (CD59 blood group) Homo sapiens 87-92 1606992-4 1992 Plasma clearance of unbound diflunisal was significantly impaired in cirrhosis: 11.5 l.min-1 in control subjects vs 7.41.min-1 in cirrhotics. Diflunisal 28-38 CD59 molecule (CD59 blood group) Homo sapiens 121-126 2338115-2 1990 The plasma clearance of diflunisal was significantly higher in men (0.169 ml.min-1.kg-1) and in women on OCS (0.165 ml.min-1.kg-1) as compared to control women (0.108 ml.min-1.kg-1). Diflunisal 24-34 CD59 molecule (CD59 blood group) Homo sapiens 77-82 2328191-4 1990 The plasma clearance of diflunisal was lowered significantly after multiple dose administration (5.2 +/- 1.2 and 4.2 +/- 0.7 ml min-1 for the 250 and 500 mg twice daily regimens, respectively) as compared with single dose administration 11.4 +/- 3.1 and 9.9 +/- 2.0 ml min-1 for the 250 and 500 mg single doses, respectively). Diflunisal 24-34 CD59 molecule (CD59 blood group) Homo sapiens 128-133 2328191-4 1990 The plasma clearance of diflunisal was lowered significantly after multiple dose administration (5.2 +/- 1.2 and 4.2 +/- 0.7 ml min-1 for the 250 and 500 mg twice daily regimens, respectively) as compared with single dose administration 11.4 +/- 3.1 and 9.9 +/- 2.0 ml min-1 for the 250 and 500 mg single doses, respectively). Diflunisal 24-34 CD59 molecule (CD59 blood group) Homo sapiens 269-274 2338115-2 1990 The plasma clearance of diflunisal was significantly higher in men (0.169 ml.min-1.kg-1) and in women on OCS (0.165 ml.min-1.kg-1) as compared to control women (0.108 ml.min-1.kg-1). Diflunisal 24-34 CD59 molecule (CD59 blood group) Homo sapiens 119-124 2338115-2 1990 The plasma clearance of diflunisal was significantly higher in men (0.169 ml.min-1.kg-1) and in women on OCS (0.165 ml.min-1.kg-1) as compared to control women (0.108 ml.min-1.kg-1). Diflunisal 24-34 CD59 molecule (CD59 blood group) Homo sapiens 119-124 2338115-4 1990 Statistically significant increases, however, were only observed for the partial metabolic clearance of diflunisal by phenolic glucuronidation between men and women (2.91 vs. 1.85 ml.min-1 respectively), and for the partial clearance by acyl glucuronidation between OCS users and control women (4.81 vs. 3.01 ml.min-1 respectively). Diflunisal 104-114 CD59 molecule (CD59 blood group) Homo sapiens 183-188 34951369-6 2021 Besides, in silico platforms have suggested that diflunisal, nabumetone, niflumic acid, and valdecoxib may be suitable for the treatment of T1DM; phenoxybenzamine and idazoxan for the treatment of T2DM by improving insulin secretion; and hydroxychloroquine reduce the risk of coronary heart disease (CHD) by counteracting inflammation. Diflunisal 49-59 insulin Homo sapiens 215-222 33806467-3 2021 This work studies the interaction of human serum albumin (HSA) with four non-steroidal anti-inflammatory drugs (NSAIDs)-ibuprofen, flurbiprofen, naproxen, and diflunisal-by monitoring the fluorescence quenching when the drug-albumin complex is formed. Diflunisal 159-169 albumin Homo sapiens 43-56 33806467-3 2021 This work studies the interaction of human serum albumin (HSA) with four non-steroidal anti-inflammatory drugs (NSAIDs)-ibuprofen, flurbiprofen, naproxen, and diflunisal-by monitoring the fluorescence quenching when the drug-albumin complex is formed. Diflunisal 159-169 albumin Homo sapiens 49-56