lte4

RG-12525（NID 525） 是一种可口服且具有选择性和竞争性的白三烯 D （LTD）拮抗剂，对 LTC4，LTD4 和 LTE4 诱导的豚鼠薄壁带收缩有抑制作用，IC50 值分别为 2.6 nM，2.5 nM 和 7 nM。RG-12525 对 CYP3A4 有抑制作用， Ki 值为 0.5 µM。RG-12525 是一种新型高效的 PPAR-γ 激动剂（IC50 值约为 60 nM），具有物种特异性，可用于研究哮喘。

AS-35 是一种可口服且具有选择性和高效性的 leukotrienes 拮抗剂，抑制 LTC4，LTD4 和 LTE4 诱导的回肠收缩。AS-35 具有抗过敏作用，抑制白三烯合成。

Leukotriene E4 (LTE4)（LTE4）通过 二肽酶对LTD4 上的作用生成，是过敏性休克慢反应物质（SRS-A）的成分之一。LTE4 存在于血浆和尿液中，可用于检测哮喘。

Tipelukast (KCA 757) 是一种新型可口服的白三烯受体 (leukotriene receptor) 拮抗剂，是具有抗炎活性，可减少纤维化，下调 TIMP-1、1 型胶原蛋白。Tipelukast 可用于研究哮喘疾病。

N-acetyl Leukotriene E4（N-乙酰白三烯 E4）是Leukotriene E4的内源性代谢物，主要通过胆汁排泄，其活性比Leukotriene E4低1~3个数量级，能引起气管的收缩。

MK 571 (L660711) 是一种具有口服活性的 CysLT1 受体拮抗剂。

Pranlukast hemihydrate (ONO-1078 hemihydrate) 是一种具有选择性和高效性的白三烯 （LT）拮抗剂，具有抗哮喘活性，抑制 [3H]LTD4 和 [3H]LTE4 与肺膜的结合，拮抗 LTC4 诱导的豚鼠气管收缩。Pranlukast hemihydrate 可用于研究哮喘。

Pranlukast (ONO-1078) 是一种半胱氨酰白三烯受体 1 拮抗剂，可拮抗或减少支气管痉挛，用于哮喘研究。

SR2640 是一种高效且高度选择性的 LTD4 LTE4 拮抗剂，以浓度依赖性方式专一抑制LTD4引发的豚鼠回肠及气管平滑肌收缩，而不影响组胺引起的收缩反应。此化合物阻止0.4 nM [3H]LTD4与豚鼠肺组织膜受体的结合，IC50为23 nM。SR2640 使得静脉注射LTD4在豚鼠中诱发的支气管收缩剂量-效应曲线平行右移，位移程度与SR2640的剂量呈正相关。SR2640 可用于哮喘研究。

LY 163443 is an dual receptor antagonist of LTD4 and LTE4.

LY 245769 is an inhibitor of leukotriene E4 (LTE4).

Leukotrienes (LTs) are a group of acute inflammatory mediators derived from arachidonic acid in leukocytes. The majority of these metabolites are formed through the 5-lipoxygenase (5-LO) pathway. 14,15-LTE4 is a metabolite of 14,15-LTC4 and 14,15-LTD4, an alternate class of LTs synthesized by a pathway involving the dual actions of 15- and 12-LOs on arachidonic acid via 15-HpETE and 14,15-LTA4 intermediates. These metabolites are classified as eoxins because they are formed mostly by eosinophils. Mast cells and nasal polyps can synthesize 14,15-LTC4 as well, however metabolism to 14,15-LTE4 in these cells and tissue has not been documented. 14,15-LTE4 increases vascular permeability of human endothelial cell monolayers with about 10-fold less potency than LTC4, but approximately 100-fold greater potency than histamine.

Slow isomerization of the C-11 double bond of LTE4 leads to the formation of 11-trans LTE4. 11-trans LTE4 is equipotent to LTE4 in contracting guinea pig ileum.

Produced by neutrophils, macrophages, mast cells, and by transcellular metabolism in platelets, leukotriene C4 (LTC4) is the parent cysteinyl leukotriene formed by the LTC4 synthase-catalyzed conjugation of glutathione to LTA4. It is one of the constituents of slow-reacting substance of anaphylaxis (SRS-A) and exhibits potent smooth muscle contracting activity. LTC4, however, is rapidly metabolized to LTD4 and LTE4, which makes the characterization of LTC4 pharmacology difficult. N-methyl Leukotriene C4 (N-methyl LTC4) is a synthetic analog of LTC4 that is not readily metabolized to LTD4 and LTE4.It acts as a potent and selective CysLT2 receptor agonist exhibiting EC50 values of 122 and > 2,000 nM at the human CysLT2 and CysLT1 receptors, respectively. It has essentially the same potency as LTC4 at both the human and murine receptors CysLT2 receptors. N-methyl LTC4 is potent and active in vivo, causing vascular leak in mice overexpressing the human CysLT2 receptor but not in CysLT2 receptor knockout mice.

LTF4 is a cysteinyl-leukotriene produced in vitro, but not reported to date in vivo. It is formed by the incubation of LTE4 with γ-glutamyl transpeptidase and glutathione. LTF4 is a weak agonist in its ability to contract vascular smooth muscle. [1] The rank order of potency of the cysteinyl-leukotrienes to contract vascular smooth muscle is LTD4 > LTC4 > LTE4 >> LTF4. [1] [2]