Leukotriene Family Related Drug Discovery Products
Creative Biolabs has the assays you can rely on for high throughput screening, lead optimization, characterizing and discovering targets, and uncovering the complexity of disease pathways. We can offer membrane protein in vitro assay kits that save valuable laboratory time and is ideal for high throughput screening.
Membrane protein stable cell lines are widely used in many areas of biomedical research. Creative Biolabs can offer membrane protein stable cell lines to stablish in vitro models for High Throughput Screening.
Creative Biolabs offers high-quality, innovative tools to help research groups accelerate membrane protein drug discovery. They can be found by targets. If there is no product that meets your needs, please contact us.
The very effective peptide-conjugated arachidonic acid-derived mediators known as cysteinyl leukotrienes (cys-LTs) are intimately connected to the pathobiology of allergic inflammation. Additionally, it is now believed that Cys-LTs contribute to the pathogenesis of cancer, fibrosis, cardiovascular disease, and immunological host defense. Therefore, each of these processes may benefit from a thorough understanding of the cellular targets and methods of action of cys-LTs.
Creative Biolabs can provide a wide variety of Leukotriene family related tools for our clients:
Overview of Leukotriene Family
Leukotrienes are inflammatory mediators produced by the arachidonic acid 5-lipoxygenase system. For the treatment of asthma, drugs that target the leukotriene pathway have been developed. The enzyme 5-lipoxygenase (5-LO) and the protein 5-LO-activating protein, which together catalyze the metabolism of endogenous arachidonic acid from membrane phospholipids to produce the unstable precursor leukotriene A4, play a significant role in both disorders. After translocation to nearby leukocytes, smooth muscle cells, endothelial cells, or platelets, LTA4 can continue to be metabolized either inside the 5-LO-expressing cell or by transcellular metabolism. Four GPCRs are involved in the leukotrienes' actions: BLT1 and BLT2, which stand for the high and low affinity receptors for LTB4, respectively; CysLT1 and CysLT2, which are activated by cysteinyl-leukotrienes.
- BLT receptor
One of the strongest leukocyte chemoattractants generated by an atherosclerotic lesion is LTB4. When LTB4 is present in nanomolar concentrations, neutrophils chemotact, however when LTB4 is present in micromolar concentrations, lysosomal enzyme release is promoted. BLT1 and BLT2, respectively, are the names of the high- and low-affinity LTB4 receptors.
- CysLT receptor
The CysLT1 and CysLT2 receptors are activated by cysteinyl-leukotrienes and are sensitive to and resistant to various antagonists that have been created to prevent leukotriene-induced bronchoconstriction. The use of CysLT1 receptor antagonists in the treatment of asthma is advantageous. B lymphocytes, eosinophils, and monocytes all express the human CysLT1 receptor, but neither T cells nor neutrophils do. Human macrophages, peripheral blood monocytes, and mast cells all express CysLT1 and CysLT2 receptors.
Fig.1 Leukotriene receptor expression in some of the target cells. (Bäck & Hansson, 2006)
Leukotriene Family Drug Discovery
LTB4 and cysteinylleukotriene release both encourage the recruitment of inflammatory cells and heighten the inflammatory response. Leukotriene receptors on vascular smooth muscle and endothelial cells also cause changes in the vascular wall's structure and function that are related to atherosclerosis. A quick exchange of information regarding atherosclerosis is made possible by the therapeutic application of leukotriene modifiers in the treatment of allergies and asthma at the moment. Leukotrienes have a role in atherosclerosis because they are locally formed within the atherosclerotic lesion and have strong pro-inflammatory effects when leukotriene receptors are activated in target cells.
Reference
- Bäck, M.; Hansson, G.K. Leukotriene receptors in atherosclerosis. Annals of medicine. 2006, 38(7): 493-502.
