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"Leukotrienes" are a family of lipid mediators derived from arachidonic acid via the action of the enzyme 5-lipoxygenase. They are not a single molecule or protein target but rather a group of signaling molecules that play key roles in inflammation and allergic responses. There are two main classes: leukotriene B₄ (LTB₄), which acts as a potent chemoattractant for neutrophils and other immune cells; and the cysteinyl leukotrienes—LTC₄, LTD₄, LTE₄—which mediate bronchoconstriction, increase vascular permeability, stimulate mucus secretion in airways, and contribute to symptoms seen in asthma and allergic diseases. Their effects are mediated through specific G protein-coupled receptors such as CYSLTR1/2 for cysteinyl leukotrienes and BLT receptors for LTB₄. Drugs targeting this pathway include receptor antagonists like montelukast or synthesis inhibitors like zileuton. "Leukotriene release" is not itself a molecular target but refers to the process by which these mediators are produced by immune cells during inflammation; thus it is an incorrect designation as a therapeutic target—it should be mapped instead to specific enzymes or receptors involved in their biosynthesis or action.[1][2][3][4] Note: The entry "Leukotriene release" is not itself a canonical molecular target but describes a biological process involving multiple molecules—primarily enzymes such as 5-lipoxygenase or receptors such as CYSLTR1/2—and should be replaced with one of those more precise targets when structuring data.[1][2]
Receptor antagonism at cysteinyl leukotriene receptors CYSLTR1 and CYSLTR2[1][2][3]; Inhibition of 5-lipoxygenase to block leukotriene synthesis[4]
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