lte4

AS-35 is an orally effective, potent, and selective antagonist of leukotrienes, antagonizing LTC4-, LTD4-, and LTE4-induced ileum contractions with IC50 values of 8 nM, 4 nM, and 3 nM, respectively. It exhibits antiallergic activities.

Tipelukast (KCA 757) is a novel, orally available leukotriene receptor antagonist with anti-inflammatory properties, capable of reducing fibrosis and down-regulating TIMP-1 and type 1 collagen. Tipelukast is utilized in asthma research.

RG-12525(NID 525) is an orally available, selective and competitive leukotriene D (LTD) antagonist that inhibits LTC4, LTD4 and LTE4-induced contraction of guinea pig thin-walled bands, with IC50 values of 2.6 nM, 2.5 nM, and 7 nM, respectively.RG-12525 inhibits CYP3A4, with a Ki value of 0.5 µM. RG-12525 is a novel and potent PPAR-γ agonist (IC50 value of about 60 nM) with species specificity for the study of asthma.

Leukotriene E4 (LTE4) (LTE4) is produced by the action of dipeptidyl peptidase on LTD4 and is a component of the Slow Reactive Substance of Anaphylaxis (SRS-A).LTE4 is present in plasma and urine and can be used to detect asthma.

Pranlukast (ONO-1078) is a cysteinyl leukotriene receptor-1 antagonist. It antagonizes or reduces bronchospasm caused, principally in asthmatics, by an allergic reaction to accidentally or inadvertently encountered allergens.

SR2640 is a potent and highly selective LTD4/LTE4 antagonist, specifically inhibiting LTD4-induced contractions in guinea pig ileum and tracheal smooth muscle in a concentration-dependent manner, without affecting histamine-induced contractions. It blocks the binding of 0.4 nM [3H]LTD4 to guinea pig lung membrane receptors with an IC50 of 23 nM. SR2640 also causes a parallel rightward shift in the dose-response curve for LTD4-induced bronchoconstriction in guinea pigs when administered intravenously, with the degree of shift correlating positively with its dosage. SR2640 is applicable for asthma research.

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.

N-acetyl Leukotriene E4 is an endogenous metabolite of Leukotriene E4, which is excreted mainly through bile, and is one to three orders of magnitude less active than Leukotriene E4, causing constriction of the airways.

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]

Pranlukast hemihydrate (ONO-1078 hemihydrate) is a selective and potent leukotriene (LT) antagonist with anti-asthmatic activity that inhibits [3H]LTD4 and [3H]LTE4 binding to lung membranes and antagonizes LTC4-induced constriction of guinea-pig airways.Pranlukast hemihydrate is used in the study of asthma. Pranlukast hemihydrate is used in the study of asthma.

MK 571 (L660711) is an orally active antagonist of CysLT1 receptor.