ライフサイエンスコーパス: niflumic acid

1 te or on CFTR, but was completely blocked by niflumic acid.

2 rent clamp, and these events were blocked by niflumic acid.

3 (DIDS), anthracene-9-carboxylate (9-AC) and niflumic acid.

4 loride transport inhibitors such as DIDS and niflumic acid.

5 amplitudes of which were reduced by A9C and niflumic acid.

6 re inhibited by the chloride channel blocker niflumic acid.

7 ne-2,2'-disulfonic acid, dithiothreitol, and niflumic acid.

8 potentiated by micromolar concentrations of niflumic acid.

9 e-2, 2'-disulfonic acid, dithiothreitol, and niflumic acid.

10 ocyanatostilbene- 2,2'-disulphonic acid) and niflumic acid.

11 This was completely inhibited by 0.5 mM niflumic acid.

12 ed by the anion transport blockers, DIDS and niflumic acid.

13 elease, as did the chloride channel blocker, niflumic acid.

14 Chloride channel blockers, niflumic acid (10 microM) and anthracene-9-carboxylic ac

15 nts that reversed at ECl and were blocked by niflumic acid (10 microM).

16 mol/L, n=5) or by the Cl- current antagonist niflumic acid (10 to 40 micromol/L, n=9).

17 ively, or Ca(2+)-dependent Cl(-) channels by niflumic acid (100 microM) did not alter Ca(2+) transien

18 ntracellular BAPTA or by bath application of niflumic acid (100 microM), a Ca(2+)-activated Cl(-) cha

19 n (220 microM), flufenamic acid (40 microM), niflumic acid (100 microM), Gd3+ (0.3 microM) or Ca2+ (2

20 anthracene-9-carboxylic acid (A9C; 1 mm) and niflumic acid (100 microm), suggesting that it was a Ca(

21 nnel blockers, glibenclamide (50 microM) and niflumic acid (100 microM).

22 ylic acid (DPC, 1 mM), DIDS (300 microM) and niflumic acid (100 microM).

23 Niflumic acid (100 mum) blocked responses to EFS but had

24 acellular Na(+) was absent, but unchanged by niflumic acid (100 mum), a Cl(-) channel blocker.

25 DAPs were inhibited by niflumic acid (125 microM) or cadmium (100 microM), and

26 Niflumic acid [2-((3-(trifluoromethyl)phenyl)amino)-3-py

27 Niflumic acid, 2-[[3-(trifluoromethyl)phenyl]amino]pyrid

28 Niflumic acid, 2-{[3-(trifluoromethyl)phenyl]amino}pyrid

29 (2,3-dimethylphenyl)aminobenzoic acid], NFA [niflumic acid; 2-{[3-(trifluoromethyl)phenyl]amino}nicot

30 tive to blockade by the Cl- channel blockers niflumic acid (300 microM) and 4,4'-diisothiocyanatostil

31 This current could be inhibited by niflumic acid (300 microM), DIDS (200 microM) and hypert

32 by SITS (0.3-1 mM), NPPB (30-300 microM) and niflumic acid (50-200 microM), but not by tamoxifen (10

33 (NPPB), N-phenylanthranilic acid (DPC), and niflumic acid (50-200 microM), known Cl- channel blocker

34 was blocked by the chloride channel blockers niflumic acid (81%) and DIDS (90%).

35 Niflumic acid, a blocker of calcium-activated chloride c

36 um channel blockers, and were potentiated by niflumic acid, an anion channel blocker.

37 ents were inhibited by 10 microM ZnCl(2) but niflumic acid, an inhibitor of Ca(2+)-activated Cl(-) ch

38 CaCC blocking drugs, niflumic acid and 4,4-diisothiocyano-2,2-stillbene-disul

39 STDs were blocked by niflumic acid and 5-nitro-2-(3-phenylpropylamino)-benzoi

40 The chloride channel blockers niflumic acid and 5-nitro-2-(3-phenylpropylamino)benzoic

41 ate free (BF) Ringer's that was inhibited by niflumic acid and by MCT siRNA knockdown, and significan

42 d by the nonspecific Cl(-) channel inhibitor niflumic acid and by preincubation with the G-protein in

43 -autocamtide-2-related inhibitory peptide or niflumic acid and CFTR(inh)-172 to WT cardiomyocytes or

44 The effects of niflumic acid and nifedipine were non-additive.

45 response was prevented by the CaCC blockers niflumic acid and T16A(inh)-A01, or by the L-type Ca(2+)

46 The addition of niflumic acid and, to a lesser extent, DIDS to the hypot

47 ) transport inhibitors (amiloride, GlyH-101, Niflumic acid) and agonists (Forskolin + IBMX, UTP).

48 el blockers 9-anthracene carboxylic acid and niflumic acid, and by its voltage-dependent kinetics.

49 NS1619, niflumic acid, and phloretin were tested by using excise

50 , and was inhibited by disulfonic stilbenes, niflumic acid, and the thiol reactive anion MTSES (Na(2-

51 ellular perfusion of the Cl- channel blocker niflumic acid but were insensitive to injection of the I

52 by NaCl, but were activated by the fenamate niflumic acid, confirming their functional expression.

53 ) and sensitivity to block by glibenclamide, niflumic acid, DIDS and extracellular ATP.

54 Under these conditions niflumic acid eliminated all OCs.

55 tive BK openers NS004 and NS1619, phloretin, niflumic acid, flufenamic acid, and 5-nitro-2-(3-phenylp

56 potency for putative Cl(-) channel blockers: niflumic acid > or = 5-nitro-2-(3-phenylpropylamino)benz

57 st of calcium-sensitive Cl- channels (CaCC), niflumic acid, had little effect on EAA release and only

58 Niflumic acid hyperpolarized Em and inhibited depolariza

59 ence that three chemically unrelated NSAIDs, niflumic acid, ibuprofen, and naproxen, acutely increase

60 ocked in a concentration-dependent manner by niflumic acid (IC(50) = 4.8 microm).

61 ecretion was abolished by the CaCC inhibitor niflumic acid in wild type and Best2(-/-) mice.

62 A reduced niflumic acid-insensitive Ca2+-activated OC persisted fo

63 e or HCO(3)(-)-rich Ringer, with and without niflumic acid (MCT inhibitor), acetazolamide (ACTZ, a CA

64 anostilbene-2,2'-disulfonic acid (DIDS), and niflumic acid (NFA) in excised inside-out and outside-ou

65 Niflumic acid (NFA), a potent blocker of Cl(Ca) in vascu

66 The effects of the Cl- channel antagonists, niflumic acid (NFA), dichloro-diphenylamine 2-carboxylic

67 yano-2,2'-disulfonic acid stilbene (DIDS) or niflumic acid (NFA).

68 Ca2+-activated Cl- channel (CLCA) inhibitor, niflumic acid (NFA, 100 microM), significantly reduced B

69 Ns treated with the anion channel inhibitors niflumic acid or 5-nitro-2-(3-phenylpropylamino)benzoic

70 arization was not inhibited by Ba2+, TEA, or niflumic acid, or altered by reduced Cl- solutions, but

71 Conversely, with charybdotoxin and niflumic acid present to inhibit K(Ca) and CI(Ca) curren

72 -clamp experiments with 4-amino-pyridine and niflumic acid present to inhibit voltage-dependent K+ (K

73 In isotonic solution, niflumic acid produced swelling, suggesting that islet C

74 , the Ca(2+)-activated Cl(-) channel blocker niflumic acid prolonged the period of oscillation only s

75 In contrast, 9AC and niflumic acid reduced the amplitude of the STDs and bloc

76 teral membrane (BL) surfaces consistent with niflumic acid-sensitive lactate-H(+) transport.

77 apical membrane were those expected of CaCC: niflumic acid sensitivity, outward rectification, and 2-

78 -activated Cl- current (ICl(Ca)) antagonist, niflumic acid, shifted the OC Vrev to ECat, suggesting t

79 Incubation with niflumic acid significantly reduced the rate of pHi chan

80 The latter two effects were reduced by niflumic acid, suggesting that taurine and hypo-osmotic

81 Niflumic acid-treated PMNs also had impaired transendoth

82 ivation of wild-type Slo2.1 currents by 3 mM niflumic acid was 14-fold greater than activation achiev

83 blocked the channel, but the blockade due to niflumic acid was less voltage-dependent than the blocka

84 yanostilbene-2,2'-disulfonic acid (DIDS) and niflumic acid were evaluated for their ability to inhibi