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1 rategies for future development of selective lipoxygenase inhibitors.
2 usly used to characterize cyclooxygenase and lipoxygenase inhibitors.
3 dependent gene expression was inhibited by 5-lipoxygenase inhibitors.
4 rious agents were given in the presence of 5-lipoxygenase inhibitors.
5 droxyl radicals, and most of them are potent lipoxygenase inhibitors.
6 ndpoints for future clinical trials of 12/15-lipoxygenase inhibitors.
7                                              Lipoxygenase inhibitors 2,3,5-trimethyl-6-(12-hydroxy-5-
8                  However, application of the lipoxygenase inhibitors 5,8,11-eicosatrienoic acid and n
9  ONO-RS-082, quinacrine and AACOCF3) and the lipoxygenase inhibitor AA861 delayed the initial outgrow
10 tor, nordihydroguaiaretic acid (NDGA), the 5-lipoxygenase inhibitor, AA861, the epoxygenase inhibitor
11 hacin was not blocked by the addition of a 5-lipoxygenase inhibitor, AA861.
12                         Phospholipase A2 and lipoxygenase inhibitors also prevented acute neurite ret
13  discussed, including combination therapies, lipoxygenase inhibitors, and lasers.
14 ygenase inhibitors, the lack of benefit from lipoxygenase inhibitors, and possible future methodologi
15                                   However, 5-lipoxygenase inhibitors, anti-IgE, and immunomodulatory
16 hes such as NO-COX-2 inhibitors and dual COX-lipoxygenase inhibitors are already warranting interest.
17               Multiple structurally distinct lipoxygenase inhibitors as well as mouse DRG neurons lac
18 mized to receive vehicle or baicalein (12/15-lipoxygenase inhibitor) at 10-15 minutes postinjury.
19  enzymes was examined in the presence of the lipoxygenase inhibitor baicalein and/or exogenous 12(S)H
20  4-aminopyridine (4-AP; 100 microM) and a 12-lipoxygenase inhibitor, baicalein (5 microM), suggesting
21                                            5-Lipoxygenase inhibitors blocked IL-16-, eotaxin-, and RA
22 bited by both nonspecific cyclooxygenase and lipoxygenase inhibitors but not by inhibitors specific f
23                       We demonstrated that 5-lipoxygenase inhibitors, but not cyclooxygenase inhibito
24                                       The 12-lipoxygenase inhibitor, cinnamyl-3,4-dihydroxy-alpha-cya
25 ects these cells from apoptosis induced by 5-lipoxygenase inhibitors, confirming a critical role of 5
26 bition of lipoxygenases because other potent lipoxygenase inhibitors failed to activate bTREK-1.
27                    Neither cyclooxygenase or lipoxygenase inhibitors had any effect on arachidonic ac
28 2+-pumping pools, whereas cyclooxygenase and lipoxygenase inhibitors had no effect.
29         This is the first study in which a 5-lipoxygenase inhibitor has been shown to attenuate exerc
30            Pharmacological intervention with lipoxygenase inhibitors may be an important new clinical
31 e cyclooxygenase inhibitor aspirin and the 5-lipoxygenase inhibitor MK-886 both partially inhibited D
32 ether inhibition of LT biosynthesis with a 5-lipoxygenase inhibitor (MK-591) induces remission in pat
33 , and treatment of these mice with the 12/15-lipoxygenase inhibitor ML-351 rescued the dysglycemic ph
34         Neither nordihydroguaiaretic acid (a lipoxygenase inhibitor) nor ethoxyresorufin (a cytochrom
35                                          The lipoxygenase inhibitor nordihydro-guaiaretic acid and th
36                           Treatment with the lipoxygenase inhibitor nordihydroguaiaretic acid (10 mic
37                                          The lipoxygenase inhibitor nordihydroguaiaretic acid, the sp
38  In this study, we examined the effects of 5-lipoxygenase inhibitors (nordihydroguaiaretic acid and A
39  addition, MA-10 cells were treated with the lipoxygenase inhibitor, nordihydroguaiaretic acid (NDGA)
40 s of superoxide-generating enzymes, only the lipoxygenase inhibitor, nordihydroguaiaretic acid reduce
41 rompted the development of a large number of lipoxygenase inhibitors of possible therapeutic and prob
42 mes; and nordihydroguaiaretic acid (NDGA), a lipoxygenase inhibitor on human lung cancer cell lines.
43 ombination with EGF, countered the effect of lipoxygenase inhibitors on PKC activation, and 12(S)HETE
44         Before initiating therapy with the 5-lipoxygenase inhibitor or placebo, only nine of 18 asthm
45  asthma received either 600 mg zileuton, a 5-lipoxygenase inhibitor, or a placebo four times daily fo
46 hibitor; PIO+ATV and zileuton, a selective 5-lipoxygenase inhibitor; or zileuton alone.
47 no bronchodilation after nine doses of the 5-lipoxygenase inhibitor (p=0.95).
48                 Nordihydroguaiaretic acid, a lipoxygenase inhibitor, prevented A23187 and exogenous A
49                                 In addition, lipoxygenase inhibitors reduce phenylephrine-induced con
50                                              Lipoxygenase inhibitors reduced the wound-induced accumu
51 viorally in rats in vivo, NRM infusion of 12-lipoxygenase inhibitors significantly reduced DOR-induce
52 The addition of nordihydroguaiaretic acid, a lipoxygenase inhibitor, significantly increased NaBT-ind
53 ction observed in various settings following lipoxygenase inhibitor treatment.
54 scovery of second generation N-hydroxyurea 5-lipoxygenase inhibitors was accomplished through the dev
55 in-treated cells, whereas cyclooxygenase and lipoxygenase inhibitors were ineffective, indicating tha
56                               Four different lipoxygenase inhibitors, which might be expected to lead
57 asthmatics and evaluate the effects of the 5-lipoxygenase inhibitor zileuton on these responses.
58                         Treatment with the 5-lipoxygenase inhibitor zileuton reduced postantigen BALF
59 that were abrogated by anti-PlGF Ab or the 5-lipoxygenase inhibitor zileuton.
60 kast, zafirlukast, and pranlukast, and the 5-lipoxygenase inhibitor, zileuton, are unique in their ab