Leukotriene B4 synthesis pathway

The **Leukotriene B4 synthesis pathway** refers to a series of enzymatic reactions that convert arachidonic acid into leukotriene B4, a potent lipid mediator involved in inflammation and immune cell recruitment. The process begins with arachidonic acid released from membrane phospholipids by phospholipase A2. The key enzyme 5-lipoxygenase, often with its activating protein FLAP, converts arachidonic acid into leukotriene A4 via intermediate steps. Leukotriene A4 is then converted to leukotriene B4 by LTA4 hydrolase[1][3][6]. This synthesized LTB4 acts as a strong chemoattractant for neutrophils and other immune cells at sites of infection or injury[1][5]. Dysregulation or overproduction of LTB4 through this biosynthetic route is implicated in various inflammatory conditions including asthma and autoimmune diseases[3][6]. **Note:** This entry describes an entire biochemical *pathway*, not a discrete molecular target such as an enzyme or receptor. Therapeutic interventions typically focus on inhibiting specific enzymes within this cascade—most notably 5-lipoxygenase or LTA4 hydrolase—rather than targeting the "Leukotriene B4 synthesis pathway" as an entity[1][3][6]. Therefore: > The term "Leukotriene B4 synthesis pathway" is **not itself considered a therapeutic target**, but rather describes the sequence of reactions leading to production of leukotriene B4. For structured data purposes, it would be more appropriate to specify individual targets within this cascade such as "Arachidonate 5-lipoxygenase" or "LTA(4) hydrolase". Drugs like zileuton inhibit 5-lipoxygenase activity and thereby block all downstream leukotrienes including LTB₄[1][3][6]. If you need information about one of these specific molecular targets instead, please clarify which enzyme or receptor you are interested in.

Other names

LTB4 biosynthesis5-lipoxygenase pathway (context-dependent)Leukotriene biosynthetic pathway