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1 low tight-binding inhibitors (alclofenac and flurbiprofen).
2 IDs) (indomethacin, ibuprofen, naproxen, and flurbiprofen).
3 d examples include a three-step synthesis of flurbiprofen.
4 ient synthesis of the anti-inflammatory drug flurbiprofen.
5 e cyclooxygenase inhibitors indomethacin and flurbiprofen.
6 nalog to share a common mode of binding with flurbiprofen.
7 on from EI* was slower for indomethacin than flurbiprofen.
8 ric COX-2 inhibitors, including naproxen and flurbiprofen.
9 ng catalysis or time-dependent inhibition by flurbiprofen.
10 cise synthesis of the anti-inflammatory drug flurbiprofen.
11 in in contrast to effects observed with ( S)-flurbiprofen.
12 iinflammatory drugs ibuprofen, naproxen, and flurbiprofen.
13 to interact directly with the carboxylate of flurbiprofen.
14 4.00-4.01 A from the heme in the presence of flurbiprofen.
15 of the non-steroidal anti-inflammatory drug flurbiprofen.
16 tion of the nonfluorescent COX inhibitor (S)-flurbiprofen.
17 ubated in the presence of the COX1 inhibitor flurbiprofen (3512+/-407 pg/ml) or the COX2 inhibitor ni
18 asis of the activation of CYP2C9-catalyzed S-flurbiprofen 4'-hydroxylation and S-naproxen O-demethyla
20 C9.1 activity as expected, CYP2C9.3-mediated flurbiprofen 4'-hydroxylation was activated in the prese
21 or were microglia activated in Tg animals by flurbiprofen (5 mg small middle dot kg(-1) small middle
22 d their numbers in S phase, suggesting that, flurbiprofen accelerates G1/S entry, and/or delays cell
24 3xTg-AD mice, we treated 3xTg-AD mice with R-flurbiprofen, an enantiomer of the NSAID flurbiprofen th
25 being 4.40 A from the heme in the absence of flurbiprofen and 4.00-4.01 A from the heme in the presen
26 ted the Type I difference spectra induced by flurbiprofen and benzbromarone, obligate anions at physi
27 uctures of PGHS-1 in complex with the NSAIDs flurbiprofen and bromoaspirin have been determined previ
28 to corroborate the relative orientations of flurbiprofen and dapsone in the active site of CYP2C9.
32 served increase in p75(NTR) protein due to R-flurbiprofen and ibuprofen treatment was accompanied by
35 in and acetaminophen and comparable with (R)-flurbiprofen and indomethacin in induction of p75NTR pro
38 tabolism by CYP3A4 and dapsone activation of flurbiprofen and naproxen metabolism by CYP2C9 were also
39 apsone increased the catalytic efficiency of flurbiprofen and naproxen oxidation by 2.3- and 16.5-fol
40 Mutagenesis of Phe114 and Phe476 abrogated flurbiprofen and naproxen oxidation, and MDS and kinetic
42 ity, including modified flurbiprofen (dimero-flurbiprofen and nitrobutyl-flurbiprofen), nabumetone (a
43 ugs (nonsteroidal anti-inflammatory drug), R-flurbiprofen and sulindac sulfide, affect only Abeta and
44 the nonsteroidal anti-inflammatory drugs (R)-flurbiprofen and sulindac sulfide, have been suggested t
46 competitive inhibitors (ibuprofen and methyl flurbiprofen) and slow tight-binding inhibitors (alclofe
49 e inhibitors ibuprofen, methyl flurbiprofen, flurbiprofen, and alclofenac at resolutions ranging from
50 ygenase inhibitors, such as indomethacin and flurbiprofen, and by replacement of heme by manganese pr
51 of three competitive inhibitors (nimesulide, flurbiprofen, and diclofenac) on the proportions and sta
54 for PGHS-2 complexed with arachidonic acid, flurbiprofen, and SC-58125 were in close agreement with
55 ne, norfluoxetine, carbamazepine, clozapine, flurbiprofen, and sulfobromophthalein did not activate t
56 compounds tested, meclofenamic acid, racemic flurbiprofen, and the purified R and S enantiomers of fl
58 roidal anti-inflammatory drugs ibuprofen and flurbiprofen), as well as mandelic acid derivatives.
59 inflammatory drugs naproxen, diclofenac, and flurbiprofen, as well as these with stearic acid in the
60 biting osteoclastic bone resorption, whereas flurbiprofen at similar concentrations was ineffective.
61 y more efficacious than the parent compound, flurbiprofen, at inhibiting osteoclast formation and bon
63 ion of benzbromarone having little effect on flurbiprofen-binding affinity in both CYP2C9.1 and CYP2C
64 is showed that while treatment of cells with flurbiprofen causes a minor change in the RNA level of d
66 f the P450 2C19 0XV complex and the P450 2C9 flurbiprofen complex differ, however, because the helix
68 glandin endoperoxide H synthase-1 (PGHS-1)/S-flurbiprofen complex suggest that the enzyme is associat
69 aglandin endoperoxide synthase-1 (PGHS-1)/S- flurbiprofen complex suggests (a) that the carboxyl grou
70 ize to that of the structure of the P450 2C9 flurbiprofen complex than to that of a modified P450 2C9
72 tment with COX-1-selective concentrations of flurbiprofen did not affect cell growth in any of the th
73 dal anti-inflammatory drugs indomethacin and flurbiprofen did not affect cytokine gene expression in
74 e cyclooxygenase inhibitors indomethacin and flurbiprofen did not hinder the early induction of c-fos
76 ave good GI tolerability, including modified flurbiprofen (dimero-flurbiprofen and nitrobutyl-flurbip
77 nonsteroidal anti-inflammatory drug (NSAID) flurbiprofen, dramatically reduced both beta-amyloid (Ab
78 cell proliferation assays have revealed that flurbiprofen effectively inhibits the growth of various
81 show in this study that indomethacin (Indo), flurbiprofen (Flur), and the selective COX-2 inhibitor N
82 omplex with the inhibitors ibuprofen, methyl flurbiprofen, flurbiprofen, and alclofenac at resolution
87 nd decreased survival, in rank-order, were R-flurbiprofen, ibuprofen, oxaprozin, fenoprofen, naproxen
88 me P450 2C9, complexed with ( S)-warfarin or flurbiprofen, implicate a cluster of three active site p
89 contained 0.014 microM CYP2C9 and 145 microM flurbiprofen in the presence and absence of 100 microM d
90 f unliganded murine COX-2 and complexes with flurbiprofen, indomethacin and SC-558, a selective COX-2
94 exhibited (S -> R) unidirectional inversion [flurbiprofen, ketoprofen, naproxen, and 2-(4-tert-butylp
95 microM, respectively) and 3-fold greater for flurbiprofen (KI* = 0.017 +/- 0.002 and 0.045 +/- 0.004
96 ental groups administered either 1) low-dose flurbiprofen (LDF) alone, 50 mg q.d.; 2) SDD (20 mg b.i.
97 fen, and the purified R and S enantiomers of flurbiprofen lowered Abeta42 levels to the greatest exte
98 to normalize levels of 2-AG suggests that R-flurbiprofen may be beneficial to treat pain in SCD, the
99 NSAIDs such as ibuprofen, indomethacin, and flurbiprofen may have direct Abeta-lowering properties i
100 th regard to CYP2C9.1- and CYP2C9.3-mediated flurbiprofen metabolism to evaluate whether the variant
102 biprofen (dimero-flurbiprofen and nitrobutyl-flurbiprofen), nabumetone (a non-acidic prodrug), and no
104 gated the effects of one of these compounds, flurbiprofen nitroxybutylester (HCT1026), on bone metabo
106 termined the effects of sulindac sulfide and flurbiprofen on gamma-cleavage of artificial constructs
107 Previously, we showed that treatment with R-flurbiprofen or ibuprofen induced p75(NTR) expression in
108 In addition, we show that treatment with R-flurbiprofen or ibuprofen led to sustained activation of
110 r, transfection of either cell line before R-flurbiprofen or ibuprofen treatment with a dominant nega
111 reated with the COX inhibitors indomethacin, flurbiprofen, or vehicle and challenged intranasally wit
114 udies revealed little change in distances of flurbiprofen protons from the heme iron of either CYP2C9
116 to evaluate the chemopreventive effects of R-flurbiprofen (R-FB), the noncyclooxygenase-inhibiting en
119 ogenous NO and PGI2 synthesis by 1-NOARG and flurbiprofen, respectively, the vasoconstriction effects
120 NO and PGI2 synthase inhibitors, 1-NOARG and flurbiprofen, respectively, were used to unmask Ang II v
124 as (+/-)-naproxen tert-butyl ester and (+/-)-flurbiprofen tert-butyl ester can be prepared in 79% and
126 h R-flurbiprofen, an enantiomer of the NSAID flurbiprofen that maintains the GSM activity but has gre
130 COX inhibitor flurbiprofen, was inhibited by flurbiprofen to about the same extent as native PGHS-2.
131 ve site with the presence of dapsone causing flurbiprofen to be oriented more closely to the heme.
133 of the non-steroidal anti-inflammatory drug, flurbiprofen, to suppress the growth of tumor cell lines
136 resonance spectroscopy (MRS) we found that R-flurbiprofen treatment decreased the elevated level of g
138 suppressor was substantially increased upon flurbiprofen treatment, yet the level of p21, a downstre
143 As observed previously with R120Q PGHS-1, flurbiprofen was an ineffective inhibitor of R120Q hPGHS
144 lts also show that for both PGHS1 and PGHS2, flurbiprofen was bound tighter to the initial EI complex
145 e structure of human P450 2C9 complexed with flurbiprofen was determined to 2.0 A by x-ray crystallog
147 R120Q subunit cannot bind the COX inhibitor flurbiprofen, was inhibited by flurbiprofen to about the
148 nly used NSAIDs, dapsone, and enantiomers of flurbiprofen were analyzed for their ability to lower th
150 effects of nonselective COX inhibition with flurbiprofen were contrasted with selective COX-2 inhibi
151 hirteen of the NSAIDs and the enantiomers of flurbiprofen were then tested in acute dosing studies in
153 -butyl esters, such as those of Naproxen and Flurbiprofen, were prepared from tert-butyl propionate a
154 ed cells from WT or Delta 18 COX-2 mice with flurbiprofen, which blocks substrate-dependent degradati
156 tudies have demonstrated that the binding of flurbiprofen with CYP2C9 is increased (decrease in K(S))
157 m-scale synthesis of medication Naproxen and Flurbiprofen with low palladium loading further highligh
158 ion of the first reversible complex (EI) for flurbiprofen with PGHS1 and PGHS2 were 0.53 +/- 0.06 and