ライフサイエンスコーパス: flufenamic acid

1 adenosine diphosphate-ribose and blocked by flufenamic acid.

2 , or the nonsteroidal anti-inflammatory drug flufenamic acid.

3 ated nonselective cation conductance blocker flufenamic acid.

4 dependent nonspecific cation current blocker flufenamic acid.

5 SCC blockers gadolinium and SKF96365 but not flufenamic acid.

6 d by the nonsteroidal anti-inflammatory drug flufenamic acid.

7 alpha- or LPS-induced NFkappaB activation by flufenamic acid.

8 d a nonselective cation current inhibited by flufenamic acid.

9 ckers of Ca(2+)-activated chloride channels, flufenamic acid (100 microM) and 9-anthracene chloride (

10 Using flufenamic acid, 2-{[3-(trifluoromethyl)phenyl]amino}ben

11 Fenamates such as FFA (flufenamic acid; 2-{[3-(trifluoromethyl)phenyl]amino}ben

12 oride (200 microM), gentamicin (220 microM), flufenamic acid (40 microM), niflumic acid (100 microM),

13 ) with N-methyl-d-glucamine and inhibited by flufenamic acid (50-200 microm), which is compatible wit

14 ro is eliminated after blockade of ICAN with flufenamic acid, 9-phenanthrol, or intracellular BAPTA.

15 er of swelling-activated Cl- channels and by flufenamic acid, a blocker of Cl- and nonselective catio

16 d the effect of PGE2 on sigh activity, while flufenamic acid, a blocker of the calcium-activated non-

17 brane changes were also largely prevented by flufenamic acid, a blocker of transient receptor potenti

18 Flufenamic acid, a nonspecific Ca2+ inhibitor, completel

19 Structural variations of flufenamic acid, a nonsteroidal anti-inflammatory drug,

20 ll-known TTR inhibitors has shown that while flufenamic acid affinity for TTR was unchanged by haloge

21 Cerebellar perfusion of flufenamic acid, an agent that restores the depolarized

22 lished the modulatory effect on sighs, while flufenamic acid, an antagonist for the calcium-activated

23 ic calcium for activation, and is blocked by flufenamic acid, an antagonist of a previously identifie

24 Flufenamic acid and 15-deoxy-Delta(12,14)-prostaglandin

25 nM) revealed a six-fold higher potency than flufenamic acid and a maximum efficacy of 129%.

26 antagonists, VRG activity was eliminated by flufenamic acid and could not be reliably restored by ad

27 s, it was possible to identify two compounds-flufenamic acid and fusidic acid-which show strong inhib

28 unction blockers (18-beta-GA, carbenoxolone, flufenamic acid and heptanol) in paired recordings.

29 ctive at depolarized voltages, stimulated by flufenamic acid and inhibited by tetraethylammonium; a v

30 Flufenamic acid and mefenamic acid are efficacious in NL

31 ting and membrane current were attenuated by flufenamic acid and SKF96365, agents known to antagonize

32 uggest that the anti-inflammatory effects of flufenamic acid and some other NSAIDs are due to their i

33 The non-specific TRP antagonist flufenamic acid and the TRPM4-specific blockers CBA and

34 Also flufenamic acid and zero external Ca2+ concentration, re

35 ng agents (carbenoxolone, octanol, heptanol, flufenamic acid, and 18alpha-glycyrrhetinic acid) with a

36 thoxyphenethyl]-1H-imidazole hydrochloride), flufenamic acid, and 2-APB (2-aminoethyl diphenylborinat

37 NS004 and NS1619, phloretin, niflumic acid, flufenamic acid, and 5-nitro-2-(3-phenylpropylamino)benz

38 junction and hemichannel inhibitors octanol, flufenamic acid, and carbenoxolone significantly blocked

39 rystal structure determination of flutamide, flufenamic acid, and cocaine, where we reduce the comput

40 blockers (heptanol, octanol, carbenoxolone, flufenamic acid, and mefloquine) are antagonists of the

41 NSAIDs, including fenoprofen, ibuprofen, and flufenamic acid, are also PPARgamma ligands and induce a

42 ve at hyperpolarized voltages, stimulated by flufenamic acid, blocked by Ba2+, and insensitive to dil

43 In that case, addition of either NPPB or flufenamic acid did not produce further inhibition.

44 ions and is inhibited by arylaminobenzoates (flufenamic acid, diphenylamine-2-carboxylate).

45 This conversion was inhibited by flufenamic acid establishing the in vivo significance of

46 ndependent and blocked by 100 microm Cd2+ or flufenamic acid (FFA) (10-200 microm), which suggests th

47 We determined the effect of flufenamic acid (FFA) and related derivatives on gap jun

48 ity Ca2+ chelator, and the I(CAN) antagonist flufenamic acid (FFA) decreased the magnitude of drive p

49 hanistic insight into the crystallization of flufenamic acid (FFA) in a confined environment of mesop

50 Flufenamic acid (FFA) is a non-steroidal anti-inflammato

51 ds such as the negatively charged activator, flufenamic acid (FFA) is critical in the search for more

52 non-steroidal anti-inflammatory drug (NSAID) flufenamic acid (FFA) is described here.

53 inution of PIP(2) reduced it; sensitivity to flufenamic acid (FFA) suggested that these effects of PI

54 We used the CAN channel blocker flufenamic acid (FFA) to examine the contribution of CAN

55 ts signaling partner gustducin, and bound to flufenamic acid (FFA), a clinically approved nonsteroida

56 stalline stages of a small organic molecule, flufenamic acid (FFA), a common pharmaceutical.

57 n in the presence of bath-applied 100 microM flufenamic acid (FFA), which attenuates a Ca(2+)-activat

58 inhibited by the connexin channel inhibitor flufenamic acid (FFA).

59 n of the nonsteroidal anti-inflammatory drug flufenamic acid (FFA; 2-{[3-(trifluoromethyl)phenyl]amin

60 r a topically applied hemichhanel inhibitor (flufenamic acid, FFA) could ameliorate the skin patholog

61 rug Administration-approved drugs, including flufenamic acid, flibanserin, and tripelennamine.

62 Here we demonstrate that flufenamic acid (Flu) inhibits the conformational change

63 Flufenamic acid, Gd(3+), La(3+) and extracellular Ca(2+)

64 Bath application of flufenamic acid, Gd3+, La3+ and Ca2+ inhibited spontaneo

65 Attenuation of amisulpride, flufenamic acid, hydrochlorothiazide, naproxen, and xipa

66 (ursodeoxycholate) and synthetic inhibitors (flufenamic acid, ibuprofen, and naproxen) was also readi

67 Finally, flufenamic acid increased SOC activity in coronary arter

68 Flufenamic acid increased the current underlying the DAP

69 Flufenamic acid inhibited spontaneous activity, but sign

70 In addition, the scale-up synthesis of flufenamic acid is also illustrated.

71 ng the non-steroidal anti-inflammatory drug, flufenamic acid is reported within the context of anti-c

72 4-methoxyphenyl)propoxy]ethyl-1H-imidazole), flufenamic acid, lanthanum, and gadolinium, consistent w

73 ructural and biophysical methods to evaluate flufenamic acid, meclofenamic acid, mefenamic acid, and

74 and UV-visible spectroscopy demonstrate that flufenamic acid, mefenamic acid, and tolfenamic acid are

75 mponent of substrate-selective inhibition by flufenamic acid, mefenamic acid, and tolfenamic acid.

76 y, we report that other fenamates, including flufenamic acid, mefenamic acid, tolfenamic acid, meclof

77 nd that was blocked by gadolinium but not by flufenamic acid or staurosporine.

78 Both gadolinium and flufenamic acid reduced I(sc) in VTC, as reported previo

79 Here, we report that flufenamic acid shows two opposing effects on COX-2 expr

80 ckers 2-APB (2-aminoethyl diphenylborinate), flufenamic acid, SKF96365 (1-[beta-[3-(4-methoxyphenyl)p

81 Our data show that flufenamic acid slows down the inactivation process of t

82 he crystal structures of cocaine, flutamide, flufenamic acid, the K salt of penicillin G, and form 4

83 tics clindamycin and tiamulin, the analgesic flufenamic acid, the musk fragrance metabolite galaxolid

84 In addition, flufenamic acid, travoprost, dutasteride, cyflumetofen,

85 The complexes from which fusidic acid and flufenamic acid were derived would not have been identif

86 The fenamates (niflumic and flufenamic acid) were found to have large effects on the