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