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1 long-acting orally active inhibitors of the LTB4 receptor.
2 oxoETEs do not appear to operate through the LTB4 receptor.
3 s, is crucial for high binding affinity with LTB4 receptors.
4 been reported to be a key binding domain to LTB4 receptors.
5 ng domain for interaction with high-affinity LTB4 receptors.
6 ase or via antagonism of the leukotriene B4 (LTB4) receptor.
7 ts of the human cell surface leukotriene B4 (LTB4) receptor.
8 ould be targeted by inhibitors of the LTB(4)-LTB4 receptor 1 (BLT1) pathway as a novel therapeutic ap
14 ice could be blocked by administration of an LTB4 receptor antagonist confirming the role of BLT1 in
15 ly inhibited by treatment with the selective LTB4 receptor antagonist CP-105,696 (ED50= 8.6 mg/kg ora
17 ffective in this regard as the pharmacologic LTB4 receptor antagonist, ONO 4057, and the blocking ant
20 sed around the high-affinity leukotriene B4 (LTB4) receptor antagonist SB 201146 (1) led to the ident
21 rt describes the synthesis of a new class of LTB4 receptor antagonists containing [2-[methyl(2-phenet
22 ction and support the clinical evaluation of LTB4 receptor antagonists in human organ transplantation
23 ationship (SAR) studies of two new series of LTB4 receptor antagonists in which the phenyl ring of th
24 may have a role in graft rejection and that LTB4 receptor antagonists may be clinically useful in th
25 (BM-DCs) express functional leukotriene B4 (LTB4) receptors as observed in dose-dependent chemotaxis
29 study demonstrates expression of functional LTB4 receptors, both BLT1 and BLT2, in murine and human
30 e reduced in mice lacking either 5-LO or the LTB4 receptor BTL1, and that macrophages from these mice
35 plays high affinity for the human neutrophil LTB4 receptor (Ki = 0.78 nM), blocks LTB4-induced Ca2+ m
37 osinophil recruitment in EAE is dependent on LTB4 receptor ligation and further reveal a previously u
39 kotrienes (LTs) or with an antagonist of the LTB4 receptor (LY223982) blocked the release of elastase
40 est that LTB4 or other potential ligands for LTB4 receptors may be important mediators of allograft r
41 e B6 mice, suggesting that expression of the LTB4 receptor on both activated autoreactive T cells and
42 leukotriene receptor-1 (BLT-1), the primary LTB4 receptor, partitioned to low density fractions, co-
43 f MIF or blockade of the MIF receptor and/or LTB4 receptor resulted in protection from LPS-induced AL
44 ngs indicate that this murine receptor is an LTB4 receptor that is highly expressed on activated leuk
46 directly inhibit LTB4 by phosphorylating the LTB4 receptor using beta adrenergic receptor kinase.